Systemic lupus erythematosus is associated with a persistent circulation of modified autoantigen-containing apoptotic debris that might be capable of breaking tolerance. We aimed to evaluate apoptotic microvesicles obtained from lupus or control mice for the presence of apoptosis-associated chromatin modifications and for their capacity to stimulate dendritic cells (DC) from lupus and control mice. Apoptotic microvesicles were in vitro generated from splenocytes, and ex vivo isolated from plasma of both MRL/lpr lupus mice and normal BALB/c mice. Microvesicles were analyzed using flow cytometry. Bone marrow-derived (BM)-DC cultured from MRL/lpr or BALB/c mice were incubated with microvesicles and CD40 expression and cytokine production were determined as measure of activation. Microvesicles derived from apoptotic splenocytes or plasma of MRL/lpr mice contained more modified chromatin compared to microvesicles of BALB/c mice, and showed enhanced activation of DC, either from MRL/lpr or BALB/c mice, and
To evaluate the role of V beta 8+ T cells in the development of lupus-like autoimmune syndrome in MRL-lpr/lpr mice, we treated them with the F23.1 anti-V beta 8 monoclonal antibody (mAb) from birth to 4 months of age. Here we report that almost complete depletion of V beta 8+ T cells by the F23.1 mAb treatment neither inhibited nor delayed the development of hypergammaglobulinemia, autoantibody production and autoimmune glomerulonephritis in MRL-lpr/lpr mice. In addition, the F23.1 mAb treatment did not prevent the development of lymphadenopathy and the generation of a CD4-CD8- double-negative T cell subset, characteristically accumulating in lpr lymph nodes. Our results strongly argue against the idea that the V beta 8+ T cells play a critical role in the development of lupus-like autoimmune syndrome in MRL-lpr/lpr mice.
Systemic lupus erythematosus is characterised by the presence of high titers of autoantibodies reacting with various components of the small and heterogeneous nuclear ribonucleoprotein particle. It has been suggested that these antibodies are produced by an antigen-driven mechanism under the dependence of antigen-specific T cells. To investigate the role of T cell help in this process, we sought with twenty overlapping peptides the Th epitopes on the U1-70K snRNP in unprimed H-2k MRL/lpr lupus mice and immunised CBA normal mice. The peptide 131-151 was recognized by both IgG autoantibodies and CD4+ T cells from 7-9 week-old MRL/lpr mice. In this test, APCs from MRL/lpr mice were required, APCs from naive CBA mice failed to stimulate CD4+ cells from MRL/lpr mice. Peptide 131-151 bound both I-Ak and I-Ek class II molecules and favoured an IL-2 positive T cell response but not IFN-γ, IL-6 and IL-10 secretion. Segment 131-151 is localised within the RNP80 motif and contains residues that are highly ...
de Lema, Guillermo Pérez, Maier, Holger, Franz, Tobias J., Escribese, Maríia, Chilla, Silvia, Segerer, Stephan, Camarasa, Natalia, Schmid, Holger, Banas, Bernhard, Kalaydjiev, Svetoslav, Busch, Dirk H., Pfeffer, Klaus, Mampaso, Francisco, Schlöndorff, Detlef und Luckow, Bruno (2005) Chemokine receptor Ccr2 deficiency reduces renal disease and prolongs survival in MRL/lpr lupus-prone mice. Journal of the American Society of Nephrology: JASN 16 (12), S. 3592-3601 ...
TY - JOUR. T1 - Mechanistic evaluation of trichloroethene-mediated autoimmune hepatitis-like disease in female MRL+/+ Mice. AU - Kondraganti, Shakuntala. AU - König, Rolf. AU - Boor, Paul J.. AU - Khan, Shahnawaz. AU - Kaphalia, Bhupendra. AU - Khan, M. AU - Ansari, Ghulam. PY - 2012. Y1 - 2012. N2 - Environmental and occupational exposure to trichloroethene (TCE) is associated with autoimmune diseases (ADs). However, the mechanisms of TCE-mediated ADs are not fully elucidated. Previous investigations showed that chronic low dose exposure of autoimmune-prone female MRL+/+ mice to TCE resulted in development of autoimmune hepatitis-like disease (AIHLD). To elucidate the mechanisms involved in the development of AIHLD, we treated female MRL+/+ mice with TCE (0.5 mg/ml) via drinking water for 24, 36 and 48 weeks. Exposure to TCE resulted in increased lymphocytic infiltration and periportal hepatocellular necrosis in the livers of mice exposed for 48 weeks. Significantly increased apoptotic cells ...
TY - JOUR. T1 - Aldosterone and prednisolone control of cochlear function in MRL/MpJ-Faslpr autoimmune mice. AU - Trune, Dennis R.. AU - Kempton, J. Beth. N1 - Funding Information: Research supported by NIH-NIDCD R01 DC03573, NIH-NIDCD R21 DC03955, and VA RR&D National Center for Rehabilitative Auditory Research RCTR 597-0160, Portland VAMC. PY - 2001. Y1 - 2001. N2 - Recently this laboratory showed aldosterone, a mineralocorticoid that only enhances sodium transport, was as effective as the glucocorticoid prednisolone in restoring cochlear function in autoimmune mice. To further test this relationship between sodium transport and autoimmune hearing loss, dosage comparisons were made of prednisolone and aldosterone control of the auditory dysfunction in autoimmune MRL/MpJ-Faslpr mice. Mice were tested at 2 months of age to establish baseline auditory brainstem response (ABR) thresholds, hematocrit, serum immune complexes, and anti-nuclear antibodies. Mice were then given different doses of ...
Click above to download a CSV file that can be opened in Excel. The file contains all strain survey measured phenotypes where this strain was tested, along with measured means and summary statistics. Field names are given in the first row. The file includes some measurement metadata fields as well as some fields related to strain means ...
The processes responsible for the production of autoantibodies have been shown to include both Ag-specific and generalized (polyclonal) forms of B cell activation. The relative contribution and temporal association of these processes to the genesis of systemic autoimmunity are incompletely understood. To study this relationship, the B cell repertoires of MRL-lpr/lpr mice were analyzed by ELISA spot assay over an 8-mo period. Between 6 and 12 wk of age, the number of splenic lymphocytes producing antibodies reactive with both autoantigens and conventional Ag increased proportionately. The repertoires of MRL-lpr/lpr mice under 12 wk were dominated by IgM-secreting B cells that showed no bias toward the production of specific autoantibodies. From 12 to 38 wk of age, an increasing proportion of animals developed repertoires dominated by IgG-secreting B cells that were skewed toward reactivity against one or very few (auto)antigens. Although there was no single Ag against which all mice developed ...
Transfer of bone marrow (BM) from autoimmunity-prone mice homozygous for the lymphoproliferation (lpr) mutation to irradiated congenic +/+ recipients has previously been shown to result in a syndrome similar to chronic graft-vs.-host (GVH) disease. It has been suggested that this syndrome may be due to an antigenic difference caused by the lpr mutation itself or to antigenic differences at loci closely linked to the lpr locus (Theofilopoulos, A. N. et al., J. Exp. Med. 1985. 162:1; Mosbach-Ozmen, L. and Loor, F., Thymus 1987. 9:197). However, the results presented here indicate that alloantigenic differences do not play a role in this syndrome. Instead, the chronic disease observed in lpr/lpr----(+/+) BM chimeras appears to develop as a result of a functional defect associated with the lpr mutation which is expressed shortly after transfer of lpr/lpr BM to irradiated recipients. This defect causes an increase in the levels of serum IgG1 and IgG2, which peak at 4-5 weeks post-transfer and
During a T cell-dependent Ab response, B cells undergo Ab class switching and V region hypermutation, with the latter process potentially rendering previously innocuous B cells autoreactive. Class switching and hypermutation are temporally and anatomically linked with both processes dependent on the enzyme, activation-induced deaminase, and occurring principally, but not exclusively, in germinal centers. To understand tolerance regulation at this stage, we generated a new transgenic mouse model expressing a membrane-tethered gamma2a-reactive superantigen (gamma2a-macroself Ag) and assessed the fate of emerging IgG2a-expressing B cells that have, following class switch, acquired self-reactivity of the Ag receptor to the macroself-Ag. In normal mice, self-reactive IgG2a-switched B cells were deleted, leading to the selective absence of IgG2a memory responses. These findings identify a novel negative selection mechanism for deleting mature B cells that acquire reactivity to self-Ag. This process ...
SLE and atherosclerosis are complex chronic inflammatory diseases characterised by immune dysfunction. Evidence supports interplay between the two diseases, with studies showing accelerated atherosclerosis in SLE. Increased activation of T cells has been demonstrated in both SLE patients and in mouse models of SLE including (NZB×NZW)F1,45 MRL/MpJ-Fas(lpr/lpr)/J46 and B6.SLE mice.24 ,27 ,28 Given the important effector and regulatory functions of T cells in atherosclerosis and that accelerated CVD is a major cause of death for SLE patients, it has been suggested that T cells may be important to consider when developing therapies for SLE and SLE-accelerated atherosclerosis (reviewed in47). However, most clinical studies to date have focused on B cells due to their role in producing the autoantibodies that lead to immune complex formation and the resultant end organ damage in SLE. The current study was undertaken to determine the effects of B6.SLE CD4+ T cells on atherosclerosis. While mice are ...
This study provides direct evidence of a promoting role for IL-17 in the pathogenesis of SLE. Although the primary physiologic role of IL-17 is to fight extracellular pathogens, increasing evidence has suggested that IL-17 can have a significant influence in the pathogenesis of several autoimmune diseases (1-4). In SLE patients, IL-17 serum levels were increased as compared with healthy control subjects (3, 17, 18). Moreover, MRLlpr/lpr and B6lpr/lpr lupus mice had high levels of IL-17 (2, 5, 19), and IL-17 could be detected in injured kidney tissues of SLE patients (6, 19). Additional data indicated that mice lacking the IL-17R had reduced humoral responses (20), and that mice lacking IL-17 were largely protected from the development of glomerulonephritis (21). Although those data underscored the proinflammatory properties of IL-17 in SLE, our findings complement and expand those observations by showing that IL-17 can directly support the propathogenic events that lead to autoantibody ...
The above data have demonstrated the critical roles of miR-7 not only in regulating PTEN expression and also B cell and Tfh cell function in lupus-prone MRL|sup|lpr/lpr|/sup| lupus mice. Furthermore, the disease manifestations in MRL|sup|lpr/lpr|/sup| lupus mice are efficiently improved by miR-7 ant …
Immunohistochemistry for p65 within glomerular lesions in MRL/lpr mice. a Control mice, b LPS-induced mice, c MP-treated mice, d SC-514-treated mice, e LPS +
3 Answers - Posted in: aciphex, gerd, doctor, medication, symptom - Answer: Aciphex (raberprazole) is a fast acting ppi that works for both lpr and ...
Anti-Sm antibodies although highly specific for systemic lupus erythematosus can only be found in 10-25% of lupus patients and lupus-prone MRL/lpr mice. Molecular studies of these autoantibodies from mice have suggested that the anti-Sm response is Ag driven, its expression is controlled by stochastic events and may originate from the same B cell precursors as anti-DNA antibodies. However, relatively little information regarding the molecular characteristics of anti-Sm antibodies in man has been reported. We studied the V region genes of three IgM hybridoma monoclonal antibodies (BUD 45.12.8, BUD 114.4.11 and BUD 94.91.8) which were selected for Sm reactivity and derived from B cells of a healthy child. Two of these antibodies BUD 45.12.8 and BUD 114.4.11 also reacted with ssDNA, while the third (BUD 94.91.8) did not. Each of these anti-Sm/RNP antibodies was encoded by different and predominantly unmutated Ig heavy chain germline genes (BUD 45.12.8 by V(H)3-23, DXP4 and J(H)4b; BUD 94.91.8 by V(H)3-33,
The potential physiological mechanisms explaining an influence of psychosocial stress on autoimmune diseases remain undetermined. Exposure of chronic social isolation stress to MRL/lpr mice significantly enhanced the degree of proteinuria after 20 weeks of age and reduced the survival rate. The seru …
Journal of Immunology Research is a peer-reviewed, Open Access journal that provides a platform for scientists and clinicians working in different areas of immunology and therapy. The journal publishes research articles, review articles, as well as clinical studies related to classical immunology, molecular immunology, clinical immunology, cancer immunology, transplantation immunology, immune pathology, immunodeficiency, autoimmune diseases, immune disorders, and immunotherapy.
TY - JOUR. T1 - Effect of late modulation of nitric oxide production on murine lupus. AU - Oates, James C.. AU - Ruiz, Philip. AU - Alexander, Audrey. AU - Pippen, Anne M.M.. AU - Gilkeson, Gary S.. PY - 1997/4. Y1 - 1997/4. N2 - MRL/MpJ-Fas(lpr) (MRL-lpr) and New Zealand Black/White (NZB/W) mice develop spontaneous autoimmune disease characterized by autoantibody production and glomerulonephritis that progresses in parallel with increasing systemic nitric oxide (NO) production. A previously published study from our laboratory indicated that oral administration of the nitric oxide synthase inhibitor N(G)-monomethyl-L-arginine (NMMA) before the onset of clinical disease significantly decreased renal and joint pathology in MRL-lpr mice. To characterize the effect of late modulation of NO production in murine SLE, we administered oral NMMA and/or restricted dietary arginine after disease onset in two murine models of SLE. When receiving combined NMMA and arginine restriction, MRL-lpr mice had ...
Given the recent success in the treatment of lupus patients with BAFF inhibitors, there is considerable interest in the lupus-like disease arising in BAFF-Tg mice. Taking advantage of the variability between 2 founder lines and gender differences in BAFF-Tg mice, we found that the tipping point for the manifestation of renal pathology and premature death was the level of BAFF protein in the serum. Slight increases in BAFF expression were sufficient to expand the B cell compartment size, yet high BAFF levels correlated with vastly increased serum IgA levels, glomerular IgA+ IC deposition, and kidney pathology. Furthermore, kidney function was improved when BAFF-Tg mice were crossed onto an IgA-deficient background. Interestingly, MRL/lpr mice with renal disease had 100-400 ng/ml BAFF in the blood (Supplemental Figure 1C), and, indeed, serum IgA levels were also elevated to about 1 mg/ml (data not shown). MRL/lpr mice are reported to have increased numbers of IgA-secreting cells, excess IgA ...
TY - JOUR. T1 - Induction of autoantibodies in normal mice by injection of nucleobindin and natural occurrence of antibodies against nucleobindin in autoimmune MRL/lpr/lpr mice. AU - Kanai, Yoshiyuki. AU - Takeda, Osamu. AU - Miura, Keiji. AU - Amagai, Mieko. AU - Kaneko, Takamasa. AU - Kubota, Tetsuo. AU - Kanai, Yukiko. AU - Tanuma, Sei ichi. AU - Kurosawa, Yoshikazu. N1 - Copyright: Copyright 2014 Elsevier B.V., All rights reserved.. PY - 1995/2. Y1 - 1995/2. N2 - Our previous works have shown that nucleobindin (Nuc) or recombinant (r) Nuc not only augments anti-DNA antibody production in vitro but also accelerates autoimmune response in vivo in MRL/+/+( MRL n) mice which are the substrain of autoimmune MRL/lpr/lpr ( MRL l) mice. To investigate whether rNuc can induce autoimmune response similarly in naive mice, we carried out intraperitoneal (i.p.) injection of rNuc (5 μg) without adjuvant into 8-week-old female BALB c mice and continued injection twice a week for 12 weeks. About 5 weeks ...
OBJECTIVES/HYPOTHESIS: The hair cells are the most vulnerable elements in the cochlea, and damage to them is the most common cause of sensorineural hearing loss. Understanding the intracellular events that lead to the death of hair cells is a key to developing protective strategies. The Fas death receptor-mediated apoptotic pathway is well studied and plays an important role in the elimination of damaged cells in a number of different cellular systems. We have studied the role of the Fas receptor in aminoglycoside-mediated toxicity in vitro. We employed the MRL/MpJ-Fas mouse, which does not express a functional Fas receptor. STUDY DESIGN: Response of Fas-deficient hair cells to gentamicin was compared with the response of normal hair cells in vitro. METHODS: Basal turn organ of Corti explants from p3-5 mice were maintained in tissue culture and treated with gentamicin for 72 hours. The explants were fixed and were stained with phalloidin, and counting was performed. RESULTS: There was no ...
Antibodies directed against IgG and DNA are found in the sera of autoimmune MRL/Mp lpr/lpr mice. Little is known of the molecular mechanisms underlying expression of such autoantibodies. We have investigated the binding diversity and pattern of VH gene expression in a panel of murine anti-IgG antibodies. We constructed eight hybridoma clones secreting IgM antibodies that bound to mouse IgG by using spleen cells from MRL/Mp lpr/lpr mice varying in age from 4 to 15 wk; one clone was derived from a 32-wk-old MRL +/+ mouse. The monoclonal IgM products exhibited varying binding specificities for intact mouse IgG, fragments of mouse IgG [Fc, Fab, (Fab)2], and heterologous IgG. Two of these antibodies crossreacted with B and/or Z DNA. Probes from seven of eight identified mouse VH gene families (7183, S107, Q52, J558, J606, 36-60, and 3609) were hybridized under high-stringency conditions with cytoplasmic RNA blots from each clone. Six clones hybridized only with the probe from the five-member 36-60 ...
MRL/Mp-(MRL/lpr) mice develop glomerular lesions with regular variants within their histopathological manifestations just like those in lupus nephritis. nephritis. MRL/lpr mice create a lethal GN with regular variants in histopathological manifestations spontaneously. These lesions may contain diffuse cell-proliferative crescentic and/or cable loop-like Praeruptorin B forms carefully resembling various aspects of human lupus nephritis [1 2 […]. ...
Interestingly, Aevm2 in an MRL allele, which governed susceptibility to vasculitis in the lower limbs with significant linkage, also showed a weak association with vasculitis in aortic branches (with a suggestive linkage in QTL analysis [LOD score 2.2]). Thus, it seems that Aevm2 might be a susceptibility locus common to vasculitis both in lower limbs and in aortic branches, although it may dominantly affect vasculitis in lower limbs. Moreover, it is worth noting that Aaom1 (13.3 cM) and Arvm1 (19.8 cM), which are the susceptibility loci to vasculitis in aortic branches and kidneys, respectively, are located close to one another on chromosome 4. This might suggest that development of vasculitis in these tissues is closely associated. However, the number of F2 mice tested in this study (n = 266) is insufficient to evaluate the statistical difference between genotype and phenotype overlap of vasculitis in each combination of tissue distribution.. We also found sex differences in the vasculitis ...
The induction of nucleoside-specific nonresponsiveness was further studied in the autoimmune strain MRL/MP +/+ (MRL/n). Experiments were undertaken to determine (i) whether nucleoside-conjugated spleen cells are able to induce specific nonresponsiveness to T-dependent nucleoside antigens in MRL/n mice, and (ii) whether periodic treatment with nucleoside-conjugated spleen cells would retard the development of spontaneous anti-DNA antibodies and associated indicators of autoimmunity. The results show that nonresponsiveness to nucleoside antigens is inducable in male, but not in female, MRL/n mice. Nonresponsiveness in male MRL/n was transferable and mediated by T cells. Treatment of male MRL/n mice with nucleoside-conjugated spleen cells (NSC) appeared to attenuate the progress of autoimmune symptoms in experimental animals. These results are discussed in the context of recent studies exploring the etiology of autoantibody production and the loss of self-tolerance in murine models of autoimmunity.
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Wing, E and Kelley, V, Loss of bacterial resistance in mrl autoimmune mice: protect- ion by prostaglandin e. Abstr. (1982). Subject Strain Bibliography 1982. 2128 ...
Methods Totally 9 mouse strains were studied including NZB, NZW, NZBW F1, MRL/lpr, MRL/Mp, BXSB/Mp, BXSB.B6.Yaa, B6.SLE1.2.3 and C57BL/6. Spleen, thymus, bone marrow and lymph node pDCs were collected from mice in different disease stages by using Nycodenz enrichment and sorting systems. Human pDCs from healthy donor and SLE patients were isolated by using BDCA4 beads selection. Mouse pDCs were stimulated with ODN2216 and Poly U for Tlr9 and Tlr7 respectively. Human pDCs were stimulated with ODN2216 and R837 for Tlr9 and Tlr7 respectively. After 18 hour for human and 36 hour for mouse, supernatant was collected for ELISA test. IFNa, TNFa, and IL6 were tested. ...
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Patients with systemic lupus erythematosus (SLE) produce more nitric oxide (NO) than controls. Furthermore, NO production correlates with disease activity measures. NO mediates inflammation through direct tissue damage and via peroxynitrite-mediated nitrosylation of key enzymes. The production of NO occurs in regions of tissue injury such as the kidney in both SLE patients and a murine lupus model: MRLllpr mice. Spontaneous NO production increases with age in MRL/lpr mice in parallel with disease activity. Blocking NO production pharmacologically ameliorates renal disease in MRLI lpr mice. We postulate that one mechanism for the excess NO production in both lupus patients and the MRL/lpr mouse is a defect in the downregulation of the iNOS inflammatory pathway. One potential mediator of downregulation of NO is the nuclear hormone receptor Peroxisome Proliferation Activated Receptor gamma (PP ARy). We and others have shown that PP ARy agonists inhibit iNOS expression and NO production by ...
One of the more profound features of systemic lupus erythematosus (SLE) is that females have a 9:1 prevalence of this disease over males. Up to 80% of SLE patients have cognitive defects or affective disorders. The mechanism of CNS injury responsible for cognitive impairment is unknown. We previously showed that ERα deficiency significantly reduced renal disease and increased survival in lupus-prone mice. We hypothesized that ERα deficiency would be similarly protective in the brain, and that ERα may play a role in modulating blood-brain barrier (BBB) integrity and/or neuroinflammation in lupus-prone mice. MRL/lpr ERα+/+ and ERαKO mice (n = 46) were ovariectomized, received 17β-estradiol pellets, and underwent radial arm water maze (WRAM) and novel object recognition (NOR) testing starting at eight weeks of age. Mice were sacrificed and brains were hemisected and processed for either immunohistochemistry, or hippocampus and parietal cortex dissection for Western blotting. MRL/lpr ERαKO mice (n =
Sister number two is a train-wreck. She is 49 and has autoimmune nephritis caused by anti GBM, an autoantibody that attacks the basement membrane in the glomerulus (kidney). She has had this for 13 years now and will hopefully be getting a kidney transplant when the time is right. Her diet is pretty restricted right now because of minimal renal function. Like many of the type Os here, she sort of ate like a vegetarian long before she became sick. Anyway, now she eats more like a type O should and does better despite eating a bit more protein for impaired renal function. She, BTW also has no weight issues either. And I suspect that she is probably an Explorer, due to many allergies to drugs and supplements. Despite having so many health issues she looks great and is able to get a good amount of exercise, but she has to avoid the sun because of a lupus like syndrome ...
A quest that began over a decade ago with a chance observation has reached a milestone: the identification of a gene that may regulate regeneration in mammals. The absence of this single gene, called p21, confers a healing potential in mice long thought to have been lost through evolution and reserved for creatures like flatworms, sponges, and some species of salamander. .... Snyder found that p21, a cell cycle regulator, was consistently inactive in cells from the MRL mouse ear. P21 expression is tightly controlled by the tumor suppressor p53, another regulator of cell division and a known factor in many forms of cancer. The ultimate experiment was to show that a mouse lacking p21 would demonstrate a regenerative response similar to that seen in the MRL mouse. And this indeed was the case. As it turned out, p21 knockout mice had already been created, were readily available, and widely used in many studies. What had not been noted was that these mice could heal their ears. ...
Further investigation revealed that the MRL mice can regenerate almost all tissues except brain. This regenerative healing is fundamentally different from normal mammalian wound healing, and takes place without scar formation (which is of particular interest to cardiologists, since scars formed in response to heart injuries, including infarcts, are probably the primary cause of subsequent chronic heart disease and failure). Such healing is known in mammals, but only very early in development - interestingly, prior to the development of certain immune, especially inflammatory, responses. Heber-Katz et al. report that T-cells from nonhealer mice do inhibit the ear wound closure response. It doesnt seem, however, that their immune dysfunction is the only mediator of the regenerative response in MRL mice. For instance, matrix metalloproteases 2 and 9 and their specific inhibitors have been shown to be differentially activated in healer vs. non-healer mice (MMPs and MMP inhibitors are primary ...
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View Psen1/Psen1 Tg(Thy1-APP)28Lpr/0 involves: 129 * C57BL/6 * CBA: phenotypes, images, diseases, and references.
I am woefully late (almost two weeks!) in getting to this (and thanks go to one of my erstwhile anonymous commenters -- for reminding me to circle back to it!), but Mercks venture-prenurial experiment for bio-similar candidates has come to an whimpering end. Merck BioVentures has been folded back into Merck Research Laboratories, and the…
TY - JOUR. T1 - Ligand recognition by anti-DNA autoantibodies. Affinity, specificity, and mode of binding. AU - Swanson, Patrick C.. AU - Ackroyd, Christine. AU - Glick, Gary D.. PY - 1996/2/6. Y1 - 1996/2/6. N2 - Understanding the molecular basis of DNA recognition by anti-DNA autoantibodies is a key element in defining the role of antibody·DNA complexes in the pathogenesis of the autoimmune disorder systemic lupus erythematosus. As part of our efforts to relate anti-DNA affinity and specificity to antibody structure, and ultimately to disease pathogenesis, we have generated a panel of eight anti-DNA mAbs from an autoimmune MRL MpJ- lpr/lpr mouse and have assessed the binding properties of these antibodies. We find that none of our anti-DNA mAbs bind to RNA and only one low-affinity mAb cross-reacts with non-DNA antigens, albeit weakly. None of the mAbs in our panel bind double-stranded DNA exclusively. Antibodies that recognize single-stranded DNA can be categorized into two groups based on ...
Previously, it was shown that TLR7-MyD88-dependent RNA sensing is absolutely crucial for the formation of Spt-GCs and the development of autoimmunity (2, 9-11). This led us to ask whether cytosolic RNA sensing by RLRs may also be equally crucial for the formation of Spt-GC responses. We also approached this study with the intention of gaining more information about how the analysis of these responses should be approached in autoimmune-prone mouse strains. Whereas endosomal TLR7-MyD88 signaling promotes Spt-GC responses in both healthy and autoimmune-prone mice on a B6 background (10), we found that cytosolic MDA5-MAVS signaling did not have a significant role in the magnitude of GC formation on a similar B6 background. More intriguingly, we found MAVS phenotypes to be dependent on the genetic background as MAVS deficiency on a B6/129 background conversely resulted in nearly absent Spt-GC responses, reminiscent of the Spt-GC responses observed in TLR7KO mice. The lack of Spt-GC response in ...
Methods for the isolation and characterization of mononuclear phagocytes from the kidneys of mice with SLE are essential to understand the patho-physiology of the disease. Activation of these cells is associated with the onset of clinical disease in mice and infiltration with these cells is associated with poor prognosis in humans.An analysis of the function of these cells should lead to a better understanding of the inflammatory processes that lead to renal impairment in SLE and other renal inflammatory diseases.
Results We found that 10% ethanol in vivo delayed disease progression and organ damage and prolonged survival. In vitro ethanol treatment not only inhibited the aggregation, proliferation, adhesion molecule expression and IFN-γ secretion of T cells, but also decreased lipid raft clustering on T cells. In addition, ethanol inhibited SLE serum-induced skin inflammation and monocyte differentiation into dendritic cells (DCs). Furthermore, ethanol treatment of monocytes that were in the process of differentiating into DCs decreased lipid raft clustering. ...
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We acknowledge support from the Center for Scientific Computing from the CNSI, MRL: an NSF MRSEC (DMR-1720256) and NSF CNS-0960316. ...
We acknowledge support from the Center for Scientific Computing from the CNSI, MRL: an NSF MRSEC (DMR-1720256) and NSF CNS-0960316. ...
Systemic lupus erythematosus is a common and often devastating systemic autoimmune disease of unknown etiology. In this communication we review the latest developments of the molecular pathogenesis of human lupus. Novel genetic studies of multiplex lupus families have revealed potential disease-associated genome intervals, put special emphasis on genetic loci mapping in the long arm of chromosome 1 and have underscored the complexity of the underlying genetic background. New data have emerged on the role of estrogens in the function of lymphocytes and a number of studies have recently emphasized the relative Th-1/Th-2 cytokine imbalance in favor of a Th-2 type cytokine immune response. Finally, novel experiments have revealed an abnormal antigen receptor- -mediated signaling process in lupus T and B cells, which may influence the aberrant expression and function of costimulatory molecules as well as of other aspects of immune cell function. It is important to decipher the underlying molecular ...
BMMSCs have been successfully utilized to treat a variety of human diseases, such as bone fracture [33], severe aplastic anemia [34], acute GVHD [13], and SLE [17]. SLE is a common and potentially fatal immune disease in which autoantibodies damage multiple organs, including the kidneys, cardiovascular system, nervous system, joints, and skin [35]. The pathology of SLE involves the destruction of targeted organ tissues and accumulation of auto-reactive lymphocytes and immune complexes. Although intensity and organ involvement vary significantly among SLE patients, abnormalities of T and B lymphocytes are universal [35-37]. Moreover, SLE provokes multifaceted immune modulation, including both deficiency and hyperactivity of the immune system. An understanding of the underlying pathology is crucial to developing optimal therapies for the restoration of immune homeostasis without compromising the protective immune responses to pathogens [38]. MRL/lpr mice were generated by the insertion of the ...
The kidney is affected to some degree in almost all patients with SLE. Renal disease is associated with higher morbidity and mortality rates. The study of the prognosis of lupus nephritis has underscored the potential importance of a number of demographic (sex, race, age), clinical, and histological parameters (WHO class, activity, and chronicity indices) which contribute to the outcome. SLE occurs more commonly in women (90%) than in men, and age at onset ranges from 16 to 50 years 8. In the present study, 89.6% of the patients with lupus nephritis were women and mean age onset of lupus nephritis was 25.8 10.2 years. Genetic factors are important in lupus nephritis, with a strong racial preponderance. The prevalence and mortality of lupus are ten times higher in black women than in whites 5. In contrast to the literature, our study showed a higher incidence of lupus nephritis among white patients (76.7%). Many clinical parameters have been used to estimate the prognosis of lupus nephritis. ...
Animals. Mice harboring the Slc39a8 conditional knockout allele C57BL/6-Slc39a8tm1.1 mrl and the constitutive knockout allele C57BL/6-Slc39a8tm1.2 mrl were provided by Merck. Details on the design of the ZIP8 mice can be found on the Taconic website (http://www.taconic.com/mouse-model/slc39a8-cko-11296 and http://www.taconic.com/mouse-model/slc39a8-ko). Briefly, the Slc39a8tm1.1 mrl allele has exon 3 flanked by loxP sites. The Slc39a8tm1.2 mrl allele was generated by Cre-mediated loxP site recombination, resulting in removal of the third exon of Slc39a8. The Slc39a8tm1.2 mrl allele deleted the N-terminal part of the ZIP domain and the first 2 transmembrane domains and generated a premature stop codon predicted to result in a protein null mouse. Alb-Cre mice, which express Cre under the control of the liver-specific albumin promoter beginning from P7, were obtained from The Jackson Laboratory (stock number 003574) and were crossed with C57BL/6-Slc39a8tm1.1 mrl mice to generate Slc39a8 ...
The answer to this question is unfortunately no. There is as of now no cure for Lupus Nephritis. The main aim of treatment is to prevent any worsening of the condition. If Lupus Nephritis is diagnosed and treated early then it may prevent the need for a kidney transplant.
Lupus Nephritis affects far more than your kidneys. Lupus Nephritis Knowledge column tells you all concerns and hot issues, such as pregnance, marriage and sexual life. Page
De-mystifying a Mysterious Disease Called Lupus Author: Mitamins Team Though many people have not even heard of Lupus, it is common - more common than some well
The heart muscle needs a constant supply of oxygen-rich blood. The coronary arteries (see Biology of the Heart and Blood Vessels: Blood Supply of the Heart),
which your article also alludes to, by saying that US citizens and LPRs cannot be denied entry under the ban. But if its not the ban, then I dont know what other US law or regulation a US citizen or LPR going to Mexico for tourism and then returning to the US would be running afoul of. By talking about a crackdown, the articles seem to imply that CBP views such travel to be somehow wrong, but I cant find anything official that says it is wrong (with respect to US law).. ...
Most people dont even know they have lupus nephritis . Despite this difficulty, Worldwide can provide you the expertise needed for your clinical trial study.
We are broadly interested in the role of commensal organisms in the development of autoimmunity. A major question in the lab is whether an autoimmune-prone host that is persistently colonized with cross-reactive commensals, develops chronic autoimmunity via molecular mimicry. We address this hypothesis using the
Cell structureCell envelopeBiosynthesis and degradation of murein sacculus and peptidoglycancell shape determining protein, MreB/Mrl family (TIGR00904; HMM-score: 39.7) ...