Mice, Inbred NZB
Antibodies, Antinuclear
Lupus Erythematosus, Systemic
Autoimmune Diseases
Lupus Nephritis
Coombs Test
Lupus Vulgaris
Mice, Inbred Strains
Autoantibodies
Anemia, Hemolytic, Autoimmune
Crosses, Genetic
Glomerulonephritis
Induction of CYP1A2 by phenobarbital in the livers of aryl hydrocarbon-responsive and -nonresponsive mice. (1/705)
The effects of phenobarbital treatment on the expression of the cytochrome P-450 (CYP or P-450) enzyme CYP1A2 in the livers of mice of various strains were examined. Phenobarbital induced the expression of CYP1A2 at the levels of mRNA, protein, and enzyme activity (methoxyresorufin O-demethylation and metabolic activation of 2-amino-3-methylimidazo[4,5-f]quinoline) in both aryl hydrocarbon-responsive [C57BL/6NCrj (C57BL/6), C3H/HeJSlc] and -nonresponsive (DBA/2NCrj, AKR/JSea, NZB/NSlc) mouse strains. The induction of CYP2B10, which is known as a phenobarbital-inducible P-450 in mice, was prominent in the livers of all five strains examined, whereas clear inductive effects on the P-450 CYP2B9 were not observed in female C57BL/6 and female DBA/2NCrj mice. These results indicate that CYP1A2 is a member of the family of phenobarbital-inducible genes in mice and suggest that the aryl hydrocarbon receptor-dependent induction pathway is not involved in the induction of CYP1A2. This concept is in accordance with those proposed by other laboratories recently using the AhR knockout mice. The following are new observations of this report. The magnitude of the increases in the CYP1A2 mRNA, protein, and enzyme activities were comparable among these three levels (ranging from 1.4- to 3. 1-fold), suggesting that the induction of CYP1A2 by phenobarbital is mainly determined at a pretranslational level. Cyclobarbital, pentobarbital, and secobarbital also induced CYP1A2 mRNA in primary culture hepatocytes from C57BL/6 mice. Barbital, in contrast, did not show any clear inductive effect on CYP1A2 mRNA. (+info)Analysis of MHC class II genes in the susceptibility to lupus in New Zealand mice. (2/705)
Hybrids of New Zealand Black (NZB) and New Zealand White (NZW) mice spontaneously develop a disease similar to human systemic lupus erythematosus. MHC and non-MHC genes contribute to disease susceptibility in this murine model. Multiple studies have shown that the NZW H2z locus is strongly associated with the development of lupus-like disease in these mice. The susceptibility gene(s) within H2z is not known, but different lines of evidence have pointed to class II MHC genes, either H2-E or H2-A (Ez or Az in NZW). Recent studies from our laboratory showed that Ez does not supplant H2z in the contribution to lupus-like disease. In the present work we generated C57BL/10 (B10) mice transgenic for Aaz and Abz genes (designated B10.Az mice) and used a (B10.Az x NZB)F1 x NZB backcross to assess the contributions of Az genes to disease. A subset of backcross mice produced high levels of IgG autoantibodies and developed severe nephritis. However, no autoimmune phenotype was linked to the Az transgenes. Surprisingly, in the same backcross mice, inheritance of H2b from the nonautoimmune B10 strain was strongly linked with both autoantibody production and nephritis. Taken together with our previous Ez studies, the present work calls into question the importance of class II MHC genes for lupus susceptibility in this model and provides new insight into the role of MHC in lupus-like autoimmunity. (+info)Vasculitis in the Palmerston North mouse model of lupus: phenotype and cytokine production profile of infiltrating cells. (3/705)
OBJECTIVE: To define the phenotype of cells in the perivascular and vascular infiltrates of Palmerston North (PN) mice and the cytokines that those cells produce. METHODS: Immunohistologic analysis, flow cytometric analysis, and reverse transcriptase-polymerase chain reaction (RT-PCR) studies were performed on tissues and cells from female PN mice and age-matched and sex-matched DBA/2 mice. RESULTS: With aging, PN mice developed a female-predominant, lupus-like disease, with a severe systemic mononuclear cell perivasculitis and vasculitis. The perivasculitis involved arteries and veins in kidney, liver, brain, and lung; the vasculitis predominantly involved veins and venules. The perivascular and vascular infiltrates in female PN mice were composed mainly of an unusual cell type that expressed phenotypic markers characteristic of both T cells (Thy1+, CD3+, CD4+, T cell receptor + [TCR+]) and B cells (B220+). In addition, the infiltrates contained a smaller number of conventional CD4+,B220- T cells and macrophages. Very few CD8+ T cells or surface Ig+ B cells were seen. Unlike the Thy1+,B220+ T cells present in MRL/lpr mice, most of which were CD4-,CD8- and TCRalpha/beta+, the majority of the Thy1+,B220+ T cells in the perivascular/vascular infiltrates of PN mice were CD4+ and expressed either TCRalpha/beta or TCRgamma/delta. By immunohistologic staining, the cells in the perivascular and vascular infiltrates in the kidneys of older PN mice were shown to produce interleukin-4 (IL-4), IL-6, and IL-10, but not IL-2, interferon-gamma, transforming growth factor beta, tumor necrosis factor alpha, or IL-1beta. By RT-PCR, the kidneys of older PN mice were found to express high levels of IL-4, IL-6, and IL-10 messenger RNA. CONCLUSION: The vascular and perivascular infiltrates in PN mice are composed predominantly of an unusual subpopulation of T cells that are Thy1+,B220+,CD4+,CD8-, express either TCRalpha/beta or TCRgamma/delta, and produce mainly type 2 cytokines. The exact role of these cells in the immunopathogenesis of lupus-like disease in PN mice remains to be elucidated. (+info)Production of high affinity autoantibodies in autoimmune New Zealand Black/New Zealand white F1 mice targeted with an anti-DNA heavy chain. (4/705)
Lupus-prone, anti-DNA, heavy (H) chain "knock-in" mice were obtained by backcrossing C57BL/6 mice, targeted with a rearranged H chain from a VH11(S107)-encoded anti-DNA hybridoma (D42), onto the autoimmune genetic background of New Zealand Black/New Zealand White (NZB/NZW) F1 mice. The targeted female mice developed typical lupus serologic manifestations, with the appearance of transgenic IgM anti-DNA autoantibodies at a young age (2-3 mo) and high affinity, somatically mutated IgM and IgG anti-DNA Abs at a later age (6-7 mo). However, they did not develop clinical, lupus-associated glomerulonephritis and survived to at least 18 mo of age. L chain analysis of transgenic anti-DNA Abs derived from diseased NZB/NZW mouse hybridomas showed a very restricted repertoire of Vkappa utilization, different from that of nonautoimmune (C57BL/6 x BALB/c)F1 transgenic anti-DNA Abs. Strikingly, a single L chain was repetitively selected by most anti-DNA, transgenic NZB/NZW B cells to pair with the targeted H chain. This L chain had the same Vkappa-Jkappa rearrangement as that expressed by the original anti-DNA D42 hybridoma. These findings indicate that the kinetics of the autoimmune serologic manifestations are similar in wild-type and transgenic lupus-prone NZB/NZW F1 mice and suggest that the breakdown of immunologic tolerance in these mice is associated with the preferential expansion and activation of B cell clones expressing high affinity anti-DNA H/L receptor combinations. (+info)Antigen-specific therapy of murine lupus nephritis using nucleosomal peptides: tolerance spreading impairs pathogenic function of autoimmune T and B cells. (5/705)
In the (SWR x NZB)F1 mouse model of lupus, we previously localized the critical autoepitopes for nephritogenic autoantibody-inducing Th cells in the core histones of nucleosomes at aa positions 10-33 of H2B and 16-39 and 71-94 of H4. A brief therapy with the peptides administered i.v. to 3-mo-old prenephritic (SWR x NZB)F1 mice that were already producing pathogenic autoantibodies markedly delayed the onset of severe lupus nephritis. Strikingly, chronic therapy with the peptides injected into 18-mo-old (SWR x NZB)F1 mice with established glomerulonephritis prolonged survival and even halted the progression of renal disease. Remarkably, tolerization with any one of the nucleosomal peptides impaired autoimmune T cell help, inhibiting the production of multiple pathogenic autoantibodies. However, cytokine production or proliferative responses to the peptides were not grossly changed by the therapy. Moreover, suppressor T cells were not detected in the treated mice. Most interestingly, the best therapeutic effect was obtained with nucleosomal peptide H416-39, which had a tolerogenic effect not only on autoimmune Th cells, but autoimmune B cells as well, because this peptide contained both T and B cell autoepitopes. These studies show that the pathogenic T and B cells of lupus, despite intrinsic defects in activation thresholds, are still susceptible to autoantigen-specific tolerogens. (+info)Splenic but not thymic autoreactive T cells from New Zealand Black mice respond to a dominant erythrocyte Band 3 peptide. (6/705)
Previous work from our laboratory suggested that erythrocyte Band 3 peptide 861-874 is the dominant epitope recognized by splenic T cells from adult New Zealand Black (NZB) mice that are developing autoimmune haemolytic anaemia (AIHA). Here, it is shown that splenic T cells from 6-week-old NZB mice mount a vigorous in vitro proliferative response to peptide 861-874 and some other selected Band 3 peptides. As the donors grow older, splenic T cells respond to an increasing number of Band 3 peptides and the magnitude of their response also becomes greater. Splenic T cells from 3-week-old NZB mice still responded vigorously to peptide 861-874 and Band 3. By contrast, neither thymocytes nor single-positive CD4-enriched thymus cells from NZB mice responded to peptide 861-874 or Band 3, although they responded to concanavalin A (Con A). However, thymocytes from mice expressing a transgenic T-cell receptor (TCR)-specific for myelin basic protein (MBP) peptide Ac 1-9 responded vigorously to Ac 1-9. It is considered that the T-cell response of NZB mice to Band 3 is initially focused on peptide 861-874 and later spreads to other Band 3 peptides as the disease progresses and that peptide 861-874-reactive T cells are primed in the periphery rather than the thymus. (+info)Genetic dissection of Sle pathogenesis: Sle3 on murine chromosome 7 impacts T cell activation, differentiation, and cell death. (7/705)
Polyclonal, generalized T cell defects, as well as Ag-specific Th clones, are likely to contribute to pathology in murine lupus, but the genetic bases for these mechanisms remain unknown. Mapping studies indicate that loci on chromosomes 1 (Sle1), 4 (Sle2), 7 (Sle3), and 17 (Sle4) confer disease susceptibility in the NZM2410 lupus strain. B6.NZMc7 mice are C57BL/6 (B6) mice congenic for the NZM2410-derived chromosome 7 susceptibility interval, bearing Sle3. Compared with B6 controls, B6.NZMc7 mice exhibit elevated CD4:CD8 ratios (2.0 vs 1.34 in 1- to 3-mo-old spleens); an age-dependent accumulation of activated CD4+ T cells (33.4% vs 21.9% in 9- to 12-mo-old spleens); a more diffuse splenic architecture; and a stronger immune response to T-dependent, but not T-independent, Ags. In vitro, Sle3-bearing T cells show stronger proliferation, increased expansion of CD4+ T cells, and reduced apoptosis (with or without anti-Fas) following stimulation with anti-CD3. With age, the B cells in this strain acquire an activated phenotype. Thus, the NZM2410 allele of Sle3 appears to impact generalized T cell activation, and this may be causally related to the low grade, polyclonal serum autoantibodies seen in this strain. Epistatic interactions with other loci may be required to transform this relatively benign phenotype into overt autoimmunity, as seen in the NZM2410 strain. (+info)Sex-limited protein: in vitro and in vivo functions. (8/705)
Mouse complement component C4 exists in two isoforms, C4 and a protein with expression restricted to male animals called sex-limited protein (Slp). Although Slp is about 95% homologous to C4, it is generally believed to be non-functional, at least in conventional haemolytic complement assays. In a previous study, however, we showed that Slp is haemolytically active in a C1-inhibitor (C1INH)-regulated, EDTA-resistant mouse complement activation pathway. To study other possible implications of this finding, we generated constitutively expressing Slp-transgenic mice. The transgene was crossed into otherwise Slp-deficient C57Bl/6J and NZB mice. Members of the third backcross generation of C57Bl/6J mice were tested for functional Slp and classical and alternative complement pathway activities (CH50 and AP50 levels, respectively). Slp-transgenic C57Bl/6J mice showed enhanced CH50, but normal AP50 levels when compared with non-transgenic littermates. To discover a possible protective role for Slp in spontaneous systemic lupus erythematosus (SLE) in NZBxNZW (NZBxW) mice, the third backcross generation of Slp-transgenic NZB mice was mated with NZW mice and the development of SLE in the female offspring was followed. In these introductory experiments, Slp-transgenic NZBxW animals presented with a significantly extended life span. Our results imply that Slp is a mouse complement component with functions which partially resemble some of those of human C4A. (+info)'NZB mice' is a term used to refer to an inbred strain of laboratory mice that are genetically identical to each other and have been used extensively in biomedical research. The 'NZB' designation stands for "New Zealand Black," which refers to the coat color of these mice.
NZB mice are known to spontaneously develop an autoimmune disease that is similar to human systemic lupus erythematosus (SLE), a chronic inflammatory disorder caused by an overactive immune system. This makes them a valuable model for studying the genetic and environmental factors that contribute to the development of SLE, as well as for testing new therapies and treatments.
It's important to note that while NZB mice are an inbred strain, they may still exhibit some variability in their disease phenotype due to genetic modifiers or environmental influences. Therefore, researchers often use large cohorts of mice and standardized experimental conditions to ensure the reproducibility and reliability of their findings.
Antinuclear antibodies (ANA) are a type of autoantibody that target structures found in the nucleus of a cell. These antibodies are produced by the immune system and attack the body's own cells and tissues, leading to inflammation and damage. The presence of ANA is often used as a marker for certain autoimmune diseases, such as systemic lupus erythematosus (SLE), Sjogren's syndrome, rheumatoid arthritis, scleroderma, and polymyositis.
ANA can be detected through a blood test called the antinuclear antibody test. A positive result indicates the presence of ANA in the blood, but it does not necessarily mean that a person has an autoimmune disease. Further testing is usually needed to confirm a diagnosis and determine the specific type of autoantibodies present.
It's important to note that ANA can also be found in healthy individuals, particularly as they age. Therefore, the test results should be interpreted in conjunction with other clinical findings and symptoms.
Systemic Lupus Erythematosus (SLE) is a complex autoimmune disease that can affect almost any organ or system in the body. In SLE, the immune system produces an exaggerated response, leading to the production of autoantibodies that attack the body's own cells and tissues, causing inflammation and damage. The symptoms and severity of SLE can vary widely from person to person, but common features include fatigue, joint pain, skin rashes (particularly a "butterfly" rash across the nose and cheeks), fever, hair loss, and sensitivity to sunlight.
Systemic lupus erythematosus can also affect the kidneys, heart, lungs, brain, blood vessels, and other organs, leading to a wide range of symptoms such as kidney dysfunction, chest pain, shortness of breath, seizures, and anemia. The exact cause of SLE is not fully understood, but it is believed to involve a combination of genetic, environmental, and hormonal factors. Treatment typically involves medications to suppress the immune system and manage symptoms, and may require long-term management by a team of healthcare professionals.
Autoimmune diseases are a group of disorders in which the immune system, which normally protects the body from foreign invaders like bacteria and viruses, mistakenly attacks the body's own cells and tissues. This results in inflammation and damage to various organs and tissues in the body.
In autoimmune diseases, the body produces autoantibodies that target its own proteins or cell receptors, leading to their destruction or malfunction. The exact cause of autoimmune diseases is not fully understood, but it is believed that a combination of genetic and environmental factors contribute to their development.
There are over 80 different types of autoimmune diseases, including rheumatoid arthritis, lupus, multiple sclerosis, type 1 diabetes, Hashimoto's thyroiditis, Graves' disease, psoriasis, and inflammatory bowel disease. Symptoms can vary widely depending on the specific autoimmune disease and the organs or tissues affected. Treatment typically involves managing symptoms and suppressing the immune system to prevent further damage.
Lupus nephritis is a type of kidney inflammation (nephritis) that can occur in people with systemic lupus erythematosus (SLE), an autoimmune disease. In lupus nephritis, the immune system produces abnormal antibodies that attack the tissues of the kidneys, leading to inflammation and damage. The condition can cause a range of symptoms, including proteinuria (protein in the urine), hematuria (blood in the urine), hypertension (high blood pressure), and eventually kidney failure if left untreated. Lupus nephritis is typically diagnosed through a combination of medical history, physical examination, laboratory tests, and imaging studies. Treatment may include medications to suppress the immune system and control inflammation, such as corticosteroids and immunosuppressive drugs.
The Coombs test is a laboratory procedure used to detect the presence of antibodies on the surface of red blood cells (RBCs). It is named after the scientist, Robin Coombs, who developed the test. There are two types of Coombs tests: direct and indirect.
1. Direct Coombs Test (DCT): This test is used to detect the presence of antibodies directly attached to the surface of RBCs. It is often used to diagnose hemolytic anemia, a condition in which RBCs are destroyed prematurely, leading to anemia. A positive DCT indicates that the patient's RBCs have been coated with antibodies, which can occur due to various reasons such as autoimmune disorders, blood transfusion reactions, or drug-induced immune hemolysis.
2. Indirect Coombs Test (ICT): This test is used to detect the presence of antibodies in the patient's serum that can agglutinate (clump) foreign RBCs. It is commonly used before blood transfusions or during pregnancy to determine if the patient has antibodies against the RBCs of a potential donor or fetus, respectively. A positive ICT indicates that the patient's serum contains antibodies capable of binding to and agglutinating foreign RBCs.
In summary, the Coombs test is a crucial diagnostic tool in identifying various hemolytic disorders and ensuring safe blood transfusions by detecting the presence of harmful antibodies against RBCs.
Lupus vulgaris is not related to systemic lupus erythematosus, which is an autoimmune disease. Instead, it's a specific form of cutaneous tuberculosis, a bacterial infection that affects the skin. It's caused by the Mycobacterium tuberculosis bacteria, the same organism responsible for pulmonary tuberculosis and other forms of tuberculosis.
Lupus vulgaris typically occurs in people who have had prior tuberculous infection or those with a weakened immune system. The condition is characterized by slowly growing, reddish-brown or violaceous papules, nodules, and plaques that may ulcerate and form scars. Lesions often have an apple jelly appearance when a glass slide is pressed against them and examined under a dermatoscope.
Lupus vulgaris lesions usually occur on the face, especially the nose, cheeks, and ears, but they can appear on other parts of the body as well. The condition can lead to significant disfigurement if left untreated. Diagnosis typically involves skin biopsy and culture or PCR for Mycobacterium tuberculosis. Treatment usually consists of a combination of multiple antituberculous drugs, such as isoniazid, rifampin, ethambutol, and pyrazinamide, along with local therapies like surgical excision or laser treatment.
Inbred strains of mice are defined as lines of mice that have been brother-sister mated for at least 20 consecutive generations. This results in a high degree of homozygosity, where the mice of an inbred strain are genetically identical to one another, with the exception of spontaneous mutations.
Inbred strains of mice are widely used in biomedical research due to their genetic uniformity and stability, which makes them useful for studying the genetic basis of various traits, diseases, and biological processes. They also provide a consistent and reproducible experimental system, as compared to outbred or genetically heterogeneous populations.
Some commonly used inbred strains of mice include C57BL/6J, BALB/cByJ, DBA/2J, and 129SvEv. Each strain has its own unique genetic background and phenotypic characteristics, which can influence the results of experiments. Therefore, it is important to choose the appropriate inbred strain for a given research question.
Autoantibodies are defined as antibodies that are produced by the immune system and target the body's own cells, tissues, or organs. These antibodies mistakenly identify certain proteins or molecules in the body as foreign invaders and attack them, leading to an autoimmune response. Autoantibodies can be found in various autoimmune diseases such as rheumatoid arthritis, lupus, and thyroiditis. The presence of autoantibodies can also be used as a diagnostic marker for certain conditions.
Hemolytic anemia, autoimmune is a type of anemia characterized by the premature destruction of red blood cells (RBCs) in which the immune system mistakenly attacks and destroys its own RBCs. This occurs when the body produces autoantibodies that bind to the surface of RBCs, leading to their rupture (hemolysis). The symptoms may include fatigue, weakness, shortness of breath, and dark colored urine. The diagnosis is made through blood tests that measure the number and size of RBCs, reticulocyte count, and the presence of autoantibodies. Treatment typically involves suppressing the immune system with medications such as corticosteroids or immunosuppressive drugs, and sometimes removal of the spleen (splenectomy) may be necessary.
"Genetic crosses" refer to the breeding of individuals with different genetic characteristics to produce offspring with specific combinations of traits. This process is commonly used in genetics research to study the inheritance patterns and function of specific genes.
There are several types of genetic crosses, including:
1. Monohybrid cross: A cross between two individuals that differ in the expression of a single gene or trait.
2. Dihybrid cross: A cross between two individuals that differ in the expression of two genes or traits.
3. Backcross: A cross between an individual from a hybrid population and one of its parental lines.
4. Testcross: A cross between an individual with unknown genotype and a homozygous recessive individual.
5. Reciprocal cross: A cross in which the male and female parents are reversed to determine if there is any effect of sex on the expression of the trait.
These genetic crosses help researchers to understand the mode of inheritance, linkage, recombination, and other genetic phenomena.
Glomerulonephritis is a medical condition that involves inflammation of the glomeruli, which are the tiny blood vessel clusters in the kidneys that filter waste and excess fluids from the blood. This inflammation can impair the kidney's ability to filter blood properly, leading to symptoms such as proteinuria (protein in the urine), hematuria (blood in the urine), edema (swelling), hypertension (high blood pressure), and eventually kidney failure.
Glomerulonephritis can be acute or chronic, and it may occur as a primary kidney disease or secondary to other medical conditions such as infections, autoimmune disorders, or vasculitis. The diagnosis of glomerulonephritis typically involves a combination of medical history, physical examination, urinalysis, blood tests, and imaging studies, with confirmation often requiring a kidney biopsy. Treatment depends on the underlying cause and severity of the disease but may include medications to suppress inflammation, control blood pressure, and manage symptoms.
Proteinuria is a medical term that refers to the presence of excess proteins, particularly albumin, in the urine. Under normal circumstances, only small amounts of proteins should be found in the urine because the majority of proteins are too large to pass through the glomeruli, which are the filtering units of the kidneys.
However, when the glomeruli become damaged or diseased, they may allow larger molecules such as proteins to leak into the urine. Persistent proteinuria is often a sign of kidney disease and can indicate damage to the glomeruli. It is usually detected through a routine urinalysis and may be confirmed with further testing.
The severity of proteinuria can vary, and it can be a symptom of various underlying conditions such as diabetes, hypertension, glomerulonephritis, and other kidney diseases. Treatment for proteinuria depends on the underlying cause and may include medications to control blood pressure, manage diabetes, or reduce protein loss in the urine.
The spleen is an organ in the upper left side of the abdomen, next to the stomach and behind the ribs. It plays multiple supporting roles in the body:
1. It fights infection by acting as a filter for the blood. Old red blood cells are recycled in the spleen, and platelets and white blood cells are stored there.
2. The spleen also helps to control the amount of blood in the body by removing excess red blood cells and storing platelets.
3. It has an important role in immune function, producing antibodies and removing microorganisms and damaged red blood cells from the bloodstream.
The spleen can be removed without causing any significant problems, as other organs take over its functions. This is known as a splenectomy and may be necessary if the spleen is damaged or diseased.
Immunoglobulin G (IgG) is a type of antibody, which is a protective protein produced by the immune system in response to foreign substances like bacteria or viruses. IgG is the most abundant type of antibody in human blood, making up about 75-80% of all antibodies. It is found in all body fluids and plays a crucial role in fighting infections caused by bacteria, viruses, and toxins.
IgG has several important functions:
1. Neutralization: IgG can bind to the surface of bacteria or viruses, preventing them from attaching to and infecting human cells.
2. Opsonization: IgG coats the surface of pathogens, making them more recognizable and easier for immune cells like neutrophils and macrophages to phagocytose (engulf and destroy) them.
3. Complement activation: IgG can activate the complement system, a group of proteins that work together to help eliminate pathogens from the body. Activation of the complement system leads to the formation of the membrane attack complex, which creates holes in the cell membranes of bacteria, leading to their lysis (destruction).
4. Antibody-dependent cellular cytotoxicity (ADCC): IgG can bind to immune cells like natural killer (NK) cells and trigger them to release substances that cause target cells (such as virus-infected or cancerous cells) to undergo apoptosis (programmed cell death).
5. Immune complex formation: IgG can form immune complexes with antigens, which can then be removed from the body through various mechanisms, such as phagocytosis by immune cells or excretion in urine.
IgG is a critical component of adaptive immunity and provides long-lasting protection against reinfection with many pathogens. It has four subclasses (IgG1, IgG2, IgG3, and IgG4) that differ in their structure, function, and distribution in the body.
List of MeSH codes (B01)
List of MeSH codes (B01) - Wikipedia
WikiGenes - Polymorphism, Restriction Fragment Length
Hyper IgE in New Zealand black mice due to a dominant-negative CD23 mutation. - MRC Weatherall Institute of Molecular Medicine
The influence of reproductive hormones on systemic lupus erythematosus
M3i - IBMC
A monoclonal antibody against a new differentiation antigen of thymoc" by C L. Sidman, L Forni et al.
Réponses antivirales chez le moustique Aedes - IBMC
Studies of consomic mice bearing the Y chromosome of the BXSB mouse. | The Journal of Immunology | American Association of...
Mice, Inbred DBA | Profiles RNS
Mice, Inbred C57BL | Profiles RNS
Mice, Inbred DBA | Profiles RNS
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Clayton K Trimmer - Research output - University of Texas Southwestern Medical Center
FITC Mouse Anti-Mouse Vβ 5.1, 5.2 T-Cell Receptor
Flashcards - Mouse Strains
Suggestive Evidence for Association of Human Chromosome 18q12-q21 and Its Orthologue on Rat and Mouse Chromosome 18 With...
MPD: Project measure / variable: Jax5 wean total
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THE MOUSE HOMOLOG TO THE RAS-RELATED YEAST GENE YPT1 MAPS ON CHROMOSOME-11 CLOSE TO THE WOBBLER (WR) LOCUS
Model Details
Free A Pocketbook Manual Of Hand And Upper Extremity Anatomy Primus Manus 2010
Pdf Per Una Storia Dell'Imposta In Italia. I Casi Della Patrimoniale E Della Nominatività Dei Titoli Al Portatore 1912 1922
Mercury exposure, malaria, and serum antinuclear/antinucleolar antibodies in amazon populations in Brazil: a cross-sectional...
Effects of the C57BL/6 strain background on tauopathy progression in the rTg4510 mouse model | Molecular Neurodegeneration |...
Lethal autoimmune hemolytic anemia in CD47-deficient nonobese diabetic (NOD) mice | Blood | American Society of Hematology
Pesquisa | Biblioteca Virtual em Saúde - BRASIL
Strains6
- Expression of the variant CD23 chain interferes with trimerisation of the receptor and has a dominant-negative effect leading to reduced IgE binding in crosses between NZB and other strains. (ox.ac.uk)
- B14-2-14 is a monoclonal cytotoxic IgM antibody which reacts with thymocytes of all mouse strains tested. (jax.org)
- One of the first INBRED MOUSE STRAINS to be sequenced. (uchicago.edu)
- Fine mapping of a major QTL influencing morphine preference in C57BL/6 and DBA/2 mice using congenic strains. (jefferson.edu)
- Highly susceptible mouse strains such as SJL/N, A.SW, B10.S (H-2 s ) develop multiple autoimmune manifestations after exposure to inorganic mercury, including lymphoproliferation, elevated levels of autoantibodies, overproduction of IgG and IgE, and circulating immune complexes in kidney and vasculature. (biomedcentral.com)
- One of the most common strains in mouse modeling is C57BL/6. (biomedcentral.com)
C57BL10
- Mice, Inbred C57BL" is a descriptor in the National Library of Medicine's controlled vocabulary thesaurus, MeSH (Medical Subject Headings) . (uchicago.edu)
- Below are the most recent publications written about "Mice, Inbred C57BL" by people in Profiles. (uchicago.edu)
- C57BL/6 lymph node cells were incubated simultaneously with FITC Mouse Anti-Mouse Vβ 5.1, 5.2 T-Cell Receptor (Cat. (bdbiosciences.com)
- Genetic transfer of the wobbler gene to a C57BL/6J x NZB hybrid stock: natural history of the motor neuron disease and response to CNTF and BDNF cotreatment. (uni-bielefeld.de)
- To determine if the phenotype of rTg4510 mice was similarly affected by the introduction of the C57BL/6 background, we compared rTg4510 mice on the original F1 FVB/N x 129S6 background to rTg4510 mice on an F1 FVB/N x C57BL/6NTac (B6/NTac) background, herein termed rTg4510 B6 . (biomedcentral.com)
- Overall, our data shows that introduction of the C57BL/6 strain into the rTg4510 mouse background modestly alters the tau pathology that was originally reported in rTg4510 on the F1 FVB/129 background. (biomedcentral.com)
- These studies support the use of the rTg4510 mouse model on a partial C57BL/6 strain background without losing fidelity of the phenotype and suggest that the C57BL/6 background does not inherently protect against tauopathy. (biomedcentral.com)
- To test the hypothesis that crossing rTg4510 mice to a C57BL/6 strain background is protective against tauopathy, we have compared rTg4510 mice on the original F1 FVB/N x 129S6 background to rTg4510 on an F1 FVB/N x C57BL/6NTac background (rTg4510 B6 ) (Figure 1 ). (biomedcentral.com)
- Breeding scheme used to produce rTg4510 mice on an F1 FVB/N x C57BL/6 (FVB/B6) strain background (rTg4510 B6 ) (Left) compared to the original rT4510 mice on an F1 FVB/N x 129S6 (FVB/129) strain background (Right). (biomedcentral.com)
- Similarly, CD47 −/− C57BL/6 mice were much more sensitive than their wild-type counterparts to experimental passive AIHA induced by anti-RBC monoclonal antibodies. (ashpublications.org)
Strain of mouse2
Phosphorylation1
- Despite a small, but significant increase in soluble human tau levels, young rTg4510 B6 mice had equivalent levels of tau phosphorylation, aggregation and cognitive impairments as age-matched rTg4510 mice. (biomedcentral.com)
Receptors1
- Antagonism of Neurotensin Receptors in the Ventral Tegmental Area Decreases Methamphetamine Self-Administration and Methamphetamine Seeking in Mice. (ouhsc.edu)
Humans1
- Kallikrein genes are associated with lupus and glomerular basement membrane-specific antibody-induced nephritis in mice and humans. (ouhsc.edu)
Chromosome6
- Studies of consomic mice bearing the Y chromosome of the BXSB mouse. (aai.org)
- Previous studies have demonstrated that the Y chromosome of the BXSB mouse can lead to accelerated autoimmunity in inbred BXSB mice and in F1 hybrids. (aai.org)
- To additionally study the effects of the BXSB-Y, we have studied three sets of Y-consomic mice, NZB.BXSB-Y, NZW.BXSB-Y, and CBA/J.BXSB-Y, each consisting of background genes from the non-BXSB parent and the Y chromosome from the BXSB mouse. (aai.org)
- Bessa?h T, de Yebenes EG, Kirkland K, Higley MJ, Buono RJ, Ferraro TN, Contreras D. Quantitative trait locus on distal chromosome 1 regulates the occurrence of spontaneous spike-wave discharges in DBA/2 mice. (jefferson.edu)
- Analysis of a quantitative trait locus for seizure susceptibility in mice using bacterial artificial chromosome-mediated gene transfer. (jefferson.edu)
- Exclusion of two candidate genes, Spnb-2 and Dcd, for the wobbler spinal muscular atrophy gene on proximal mouse chromosome 11. (uni-bielefeld.de)
Transgenic5
- This strain is commonly used as genetic background for transgenic mouse models. (uchicago.edu)
- Cross-breeding of transgenic mice is commonly used to assess gene-gene interactions, particularly in the context of disease. (biomedcentral.com)
- Non-transgenic (NT) littermates of rTg4510 B6 (NT B6 ) mice also had greater amounts of cortical and hippocampal phospho-tau at 10.5 months of age when compared to NT littermates of rTg4510 mice. (biomedcentral.com)
- Numerous transgenic mice expressing wild-type or mutant human tau have been created to model the neuropathology of tauopathies-a group of neurodegenerative diseases characterized by the accumulation of tau protein aggregates. (biomedcentral.com)
- The strain background of transgenic mice can also alter disease progression and presentation. (biomedcentral.com)
Congenic1
- Using congenic mice, we have determined that genes on Chrs. (dyslexialab.net)
Spontaneously1
- We show here that virtually all CD47-deficient nonobese diabetic (NOD) mice spontaneously develop severe lethal autoimmune hemolytic anemia (AIHA) at 180 to 280 days of age, whereas none of the control CD47 + NOD mice develop lethal AIHA at least during the first year of life. (ashpublications.org)
Susceptible2
- Using knock-out and B-cell-conditional knock-out murine models, we identify Carabin as a new negative regulator of B-cell function, whose deficiency in B cells speeds up early B-cell responses and makes the mice more susceptible to anti-dsDNA production and renal lupus flare after stimulation with a Toll-like Receptor 9 agonist, CpG-DNA. (cnrs.fr)
- Potassium channel activity and glutamate uptake are impaired in astrocytes of seizure-susceptible DBA/2 mice. (jefferson.edu)
Nude1
- In the periphery, the antigen is found on a few percent of lymph node and not on splenic T cells, and it is absent in nude mice. (jax.org)
Additionally1
- Additionally, older rTg4510 B6 mice had gross forebrain neurodegeneration that was equivalent to age-matched rTg4510 mice. (biomedcentral.com)
Microbiota3
- Gut microbiota modulates bleomycin-induced acute lung injury response in mice. (uchicago.edu)
- Previously, using lupus-prone (SWR × NZB)F1 (SNF1) mice, we have shown that the intestinal immune system could play a role in the initiation and progression of disease in SLE, and depletion of gut microbiota produces more pronounced disease protection in females than in males. (bvsalud.org)
- Furthermore, we observed that the disease protection achieved in female SNF1 mice upon depletion of gut microbiota correlates with the diminished gut inflammatory protein levels, intestinal permeability and circulating microbial DNA levels. (bvsalud.org)
Model4
- Here, we show that Carabin is low in B cells of (NZB × NZW) F1 mice (murine SLE model) long before the disease onset, and is low in B cells of lupus patients during the inactive phases of the disease. (cnrs.fr)
- Retinal ganglion cell protection by 17-beta-estradiol in a mouse model of inherited glaucoma. (ouhsc.edu)
- Single CAR-T cell treatment controls disseminated ovarian cancer in a syngeneic mouse model. (uchicago.edu)
- We sought to determine if changing the strain background of a commonly used mouse model of tauopathy (rTg4510) would significantly impact the originally reported phenotype. (biomedcentral.com)
Gene4
- Identification of five mouse mu-opioid receptor (MOR) gene (Oprm1) splice variants containing a newly identified alternatively spliced exon. (jefferson.edu)
- These gene loci are deleted in mice having the a (e.g. (bdbiosciences.com)
- Spinal muscular atrophy gene wobbler of the mouse: evidence from chimeric spinal cord and testis for cell-autonomous function. (uni-bielefeld.de)
- Meis1, a PBX1-related homeobox gene involved in myeloid leukemia in BXH-2 mice. (uni-bielefeld.de)
Genes1
- Characterization of genes expressed early in mouse spermatogenesis, isolated from a subtractive cDNA library. (uni-bielefeld.de)
Responses1
- The IgE response is in turn regulated by the B-cell co-receptor CD23, and CD23-deficient mice show exaggerated IgE responses and airway hyper-responsiveness. (ox.ac.uk)
Results2
- These results suggest that NZB mice or mice carrying the variant allele will be useful models for studying both allergy and quantitative traits associated with atopy. (ox.ac.uk)
- Neurotropin happens the disastrous able figures of NZB results. (fleamarketpost.com)
Previously reported1
- In contrast, NZW.BXSB-Y males had accelerated renal and cardiac disease and early death, resembling that previously reported for (NZW X BXSB)F1 mice. (aai.org)
Natural1
- The exaggerated IgE response provides an explanation for the natural resistance of NZB mice to parasitic infection by Leishmania. (ox.ac.uk)
Black2
- Hyper IgE in New Zealand black mice due to a dominant-negative CD23 mutation. (ox.ac.uk)
- In this report, we show that New Zealand black (NZB) mice express a variant CD23 allele, with mutations in both the C-lectin-binding domain and stalk region, which fails to bind IgE at high affinity and has reduced expression on the cell surface. (ox.ac.uk)
Levels1
- Here, we show that the gut permeability features of lupus-prone female SNF1 mice at juvenile ages directly correlate with the expression levels of pro-inflammatory factors, faecal IgA abundance and nAg reactivity and the eventual systemic autoantibody levels and proteinuria onset. (bvsalud.org)
Long1
- They lived almost as long as NZB mice. (aai.org)
Effects1
- Effects of Depilatory Cream Formulation and Contact Time on Mouse Skin. (uchicago.edu)
Presence2
- The presence of the BXSB-Y in all of the consomic mice was confirmed by crossing the consomic mice with BXSB females and demonstrating accelerated disease in the male offspring. (aai.org)
- 4 and 8 of the mouse modulate the presence of spontaneous malformations. (dyslexialab.net)
Cells1
- Foxe1 Deletion in the Adult Mouse Is Associated With Increased Thyroidal Mast Cells and Hypothyroidism. (uchicago.edu)
Year1
- This graph shows the total number of publications written about "Mice, Inbred DBA" by people in this website by year, and whether "Mice, Inbred DBA" was a major or minor topic of these publications. (ouhsc.edu)
Factor1
- Anti-inflammatory effect of pigment epithelium-derived factor in DBA/2J mice. (ouhsc.edu)
Models2
- Immunoglobulin G subclasses confer protection against Staphylococcus aureus bloodstream dissemination through distinct mechanisms in mouse models. (uchicago.edu)
- Strain background changes can influence the phenotype of mouse models and can confound crossbreeding studies. (biomedcentral.com)
Original1
- On the original F1 FVB/N x 129S6 background, rTg4510 mice present with progressive cognitive decline, increased insoluble tau, robust tau pathology and age-dependent neurodegeneration. (biomedcentral.com)
Control1
- We found that the CBA/J.BXSB-Y mice showed few differences from control CBA/J males. (aai.org)
Analysis1
- Systems genetics analysis of mouse chondrocyte differentiation. (jefferson.edu)
Background1
- Here we compare the phenotypes of both young and old rTg4510 mice on each strain background. (biomedcentral.com)