Immune System Phenomena
Immune System
Raynaud Disease
Scleroderma, Localized
Pruritus
Scleroderma, Systemic
CREST Syndrome
Scleroderma, Diffuse
Opportunistic autoimmune disorders: from immunotherapy to immune dysregulation. (1/10)
(+info)Inhibitory RNA molecules in immunotherapy for cancer. (2/10)
(+info)The ancestry and cumulative evolution of immune reactions. (3/10)
The last two decades of study enriched greatly our knowledge of how the immune system originated and the sophisticated immune mechanisms of today's vertebrates and invertebrates developed. Even unicellular organisms possess mechanisms for pathogen destruction and self recognition. The ability to distinguish self from non-self is a prerequisite for recognition of sexual compatibility and ensuring survival. Molecules involved in these processes resemble those found in the phagocytic cells of higher organisms. Recognition of bacteria by scavenger receptors induces phagocytosis or endocytosis. The phagocytic mechanisms characterizing the amoeboid protozoans developed further during the evolution towards innate immunity. The scavenger receptor cysteine-rich domain SRCR is encoded in the genomes from the most primitive sponges to mammals. The immune system of sponges comprises signal transduction molecules which occur in higher metazoans as well. Sponges already possess recognition systems for pathogenic bacteria and fungi, based on membrane receptors (a lipopolysaccharide-interacting protein, a cell surface receptor recognizing beta(1 --> 3)-d-glucans of fungi). Perforin-like molecules and lysozymes are involved, among others, in defense in sponges. Reactive oxygen and nitrogen species function in the immunity of early metazoan. Genes encoding the family of reactive oxygen-generating NADPH oxidases (Noxes) are found in a variety of protists and plants. The NO synthases of cnidarians, mollusks, and chordates are conserved with respect to the mammalian NOS. The antimicrobial peptides of protozoans, amoebapores, are structural and functional analogs of the natural killer cell peptide, NK-lysin, of vertebrates. An ancestral S-type lectin has been found in sponges. Opsonizing properties of lectins and the ability to agglutinate cells justify their classification as primitive recognition molecules. Invertebrate cytokines are not homologous to those of vertebrate, and their functional convergence was presumably enabled by the general similarity of the lectin-like recognition domain three-dimensional structure. Sponges contain molecules with SCR/CCP domains that show high homology to the mammalian regulators of complement activation (RCA family). A multi-component complement system comprising at least the central molecule of the complement system, C3, Factor B, and MASP developed in the cnidarians and evolved into the multilevel cascade engaged in innate and acquired immunity of vertebrates. The adaptive immune system of mammals is also deeply rooted in the metazoan evolution. Some its precursors have been traced as deep as in sponges, namely, two classes of receptors that comprise Ig-like domains, the receptor tyrosine kinases (RTK), and the non-enzymic sponge adhesion molecules (SAM). The antibody-based immune system defined by the presence of the major histocompatibility complex (MHC), T-cell receptor (TCR), B-cell receptor (BCR) or recombination activating genes (RAGs) is known beginning from jawed fishes. However, genes closely resembling RAG1 and RAG2 have been uncovered in the genome of a see urchin. The ancestry of MHC gene remains unknown. Similarly, no homologue of the protein binding domain (PBD) in MHC molecules has been found in invertebrates. The pathway by which endogenous peptides are degraded for presentation with class I MHC molecules utilizes mechanisms similar to those involved in the normal turnover of intracellular proteins, apparently recruited to work also for the immune system. Several cDNAs coding for lysosomal enzymes, e.g., cathepsin, have been isolated from sponges. All chromosomal duplication events in the MHC region occurred after the origin of the agnathans but before the gnathostomes split from them. The V-domains of the subtype found in the receptors of T and B-cells are known from both agnathans and cephalochordates, although they do not rearrange. The rearrangement mechanism of the lymphocyte V-domains suggests its origin from a common ancestral domain existing before the divergence of the extant gnathostome classes. Activation-induced deaminase (AID) - homologous proteins have been found only in the gnathostomes. It appears thus that the adaptive immunity of vertebrates is a result of stepwise accumulation of small changes in molecules, cells and organs over almost half a billion years. (+info)Ncf1 (p47phox) is essential for direct regulatory T cell mediated suppression of CD4+ effector T cells. (4/10)
(+info)IL-17A-dependent CD4+CD25+ regulatory T cells promote immune privilege of corneal allografts. (5/10)
(+info)Role of notch signaling in osteoimmunology--from the standpoint of osteoclast differentiation. (6/10)
(+info)Computational approaches to understanding dendritic cell responses to influenza virus infection. (7/10)
(+info)Evolution of vertebrate immunity. (8/10)
(+info)Immune system phenomena refer to the various observable events and processes that occur in the context of the immune system's response to foreign substances or organisms (such as bacteria, viruses, parasites, or fungi) that invade the body, as well as its response to abnormal cells like cancer cells. These phenomena can include a range of responses, such as:
1. Inflammation: This is the body's response to tissue damage, which can be caused by infection or injury. It involves the recruitment of immune cells to the site of damage, increased blood flow, and the release of various chemical mediators.
2. Antigen presentation: This is the process by which the immune system identifies foreign substances. Antigens are presented to immune cells (like T-cells) by specialized cells (like dendritic cells), which helps trigger an immune response.
3. Activation of immune cells: Various signals can lead to the activation of different types of immune cells, such as B-cells, T-cells, and phagocytes. Once activated, these cells can perform various functions, such as producing antibodies or engulfing and destroying foreign substances.
4. Antibody production: B-cells produce antibodies, which are proteins that recognize and bind to specific antigens. This binding can neutralize the antigen, mark it for destruction, or help activate other immune cells.
5. Cell-mediated immunity: This is a type of immunity that involves the activation of T-cells, which can directly attack infected cells or help coordinate the immune response.
6. Hypersensitivity reactions: These are abnormal or exaggerated immune responses to harmless substances, which can cause tissue damage and inflammation. There are four types of hypersensitivity reactions (type I-IV), each with different mechanisms and characteristics.
7. Autoimmunity: This is a phenomenon in which the immune system mistakenly attacks the body's own cells and tissues, leading to chronic inflammation and tissue damage.
8. Immunodeficiency: This refers to a state in which the immune system is weakened or compromised, making an individual more susceptible to infections and diseases.
9. Tolerance: This is a state in which the immune system learns to recognize and tolerate harmless substances, preventing unnecessary immune responses and inflammation.
10. Immunological memory: This is the ability of the immune system to remember previous encounters with pathogens or antigens, allowing for faster and more effective responses upon subsequent exposures.
The immune system is a complex network of cells, tissues, and organs that work together to defend the body against harmful invaders. It recognizes and responds to threats such as bacteria, viruses, parasites, fungi, and damaged or abnormal cells, including cancer cells. The immune system has two main components: the innate immune system, which provides a general defense against all types of threats, and the adaptive immune system, which mounts specific responses to particular threats.
The innate immune system includes physical barriers like the skin and mucous membranes, chemical barriers such as stomach acid and enzymes in tears and saliva, and cellular defenses like phagocytes (white blood cells that engulf and destroy invaders) and natural killer cells (which recognize and destroy virus-infected or cancerous cells).
The adaptive immune system is more specific and takes longer to develop a response but has the advantage of "remembering" previous encounters with specific threats. This allows it to mount a faster and stronger response upon subsequent exposures, providing immunity to certain diseases. The adaptive immune system includes T cells (which help coordinate the immune response) and B cells (which produce antibodies that neutralize or destroy invaders).
Overall, the immune system is essential for maintaining health and preventing disease. Dysfunction of the immune system can lead to a variety of disorders, including autoimmune diseases, immunodeficiencies, and allergies.
Raynaud's disease, also known as Raynaud's phenomenon or syndrome, is a condition that affects the blood vessels, particularly in the fingers and toes. It is characterized by episodes of vasospasm (constriction) of the small digital arteries and arterioles, which can be triggered by cold temperatures or emotional stress. This results in reduced blood flow to the affected areas, causing them to become pale or white and then cyanotic (blue) due to the accumulation of deoxygenated blood. As the episode resolves, the affected areas may turn red as blood flow returns, sometimes accompanied by pain, numbness, or tingling sensations.
Raynaud's disease can be primary, meaning it occurs without an underlying medical condition, or secondary, which is associated with connective tissue disorders, autoimmune diseases, or other health issues such as carpal tunnel syndrome, vibration tool usage, or smoking. Primary Raynaud's is more common and tends to be less severe than secondary Raynaud's.
Treatment for Raynaud's disease typically involves avoiding triggers, keeping the body warm, and using medications to help dilate blood vessels and improve circulation. In some cases, lifestyle modifications and smoking cessation may also be recommended to manage symptoms and prevent progression of the condition.
Localized scleroderma, also known as morphea, is a rare autoimmune disorder that affects the skin and connective tissues. It is characterized by thickening and hardening (sclerosis) of the skin in patches or bands, usually on the trunk, limbs, or face. Unlike systemic scleroderma, localized scleroderma does not affect internal organs, although it can cause significant disfigurement and disability in some cases.
There are two main types of localized scleroderma: plaque morphea and generalized morphea. Plaque morphea typically presents as oval or circular patches of thickened, hard skin that are often white or pale in the center and surrounded by a purple or darker border. Generalized morphea, on the other hand, is characterized by larger areas of sclerosis that can cover much of the body surface.
The exact cause of localized scleroderma is not fully understood, but it is thought to involve an overactive immune system response that leads to inflammation and scarring of the skin and underlying tissues. Treatment typically involves a combination of topical therapies (such as corticosteroids or calcineurin inhibitors), phototherapy, and systemic medications (such as methotrexate or mycophenolate mofetil) in more severe cases.
Pruritus is a medical term derived from Latin, in which "prurire" means "to itch." It refers to an unpleasant sensation on the skin that provokes the desire or reflex to scratch. This can be caused by various factors, such as skin conditions (e.g., dryness, eczema, psoriasis), systemic diseases (e.g., liver disease, kidney failure), nerve disorders, psychological conditions, or reactions to certain medications.
Pruritus can significantly affect a person's quality of life, leading to sleep disturbances, anxiety, and depression. Proper identification and management of the underlying cause are essential for effective treatment.
Systemic Scleroderma, also known as Systemic Sclerosis (SSc), is a rare, chronic autoimmune disease that involves the abnormal growth and accumulation of collagen in various connective tissues, blood vessels, and organs throughout the body. This excessive collagen production leads to fibrosis or scarring, which can cause thickening, hardening, and tightening of the skin and damage to internal organs such as the heart, lungs, kidneys, and gastrointestinal tract.
Systemic Scleroderma is characterized by two main features: small blood vessel abnormalities (Raynaud's phenomenon) and fibrosis. The disease can be further classified into two subsets based on the extent of skin involvement: limited cutaneous systemic sclerosis (lcSSc) and diffuse cutaneous systemic sclerosis (dcSSc).
Limited cutaneous systemic sclerosis affects the skin distally, typically involving fingers, hands, forearms, feet, lower legs, and face. It is often associated with Raynaud's phenomenon, calcinosis, telangiectasias, and pulmonary arterial hypertension.
Diffuse cutaneous systemic sclerosis involves more extensive skin thickening and fibrosis that spreads proximally to affect the trunk, upper arms, thighs, and face. It is commonly associated with internal organ involvement, such as interstitial lung disease, heart disease, and kidney problems.
The exact cause of Systemic Scleroderma remains unknown; however, it is believed that genetic, environmental, and immunological factors contribute to its development. There is currently no cure for Systemic Scleroderma, but various treatments can help manage symptoms, slow disease progression, and improve quality of life.
CREST syndrome is a subtype of a autoimmune connective tissue disorder called scleroderma (systemic sclerosis). The name "CREST" is an acronym that stands for the following five features:
* Calcinosis: The formation of calcium deposits in the skin and underlying tissues, which can cause painful ulcers.
* Raynaud's phenomenon: A condition in which the blood vessels in the fingers and toes constrict in response to cold or stress, causing the digits to turn white or blue and become numb or painful.
* Esophageal dysmotility: Difficulty swallowing due to weakened muscles in the esophagus.
* Sclerodactyly: Thickening and tightening of the skin on the fingers.
* Telangiectasias: Dilated blood vessels near the surface of the skin, causing red spots or lines.
It's important to note that not everyone with CREST syndrome will have all five of these features, and some people may have additional symptoms not included in the acronym. Additionally, CREST syndrome is a chronic condition that can cause a range of complications, including lung fibrosis, kidney problems, and digital ulcers. Treatment typically focuses on managing specific symptoms and slowing the progression of the disease.
Diffuse scleroderma is a medical condition that falls under the systemic sclerosis category of autoimmune rheumatic diseases. It is characterized by thickening and hardening (sclerosis) of the skin and involvement of internal organs. In diffuse scleroderma, the process affects extensive areas of the skin and at least one internal organ.
The disease process involves an overproduction of collagen, a protein that makes up connective tissues in the body. This excessive collagen deposition leads to fibrosis (scarring) of the skin and various organs, including the esophagus, gastrointestinal tract, heart, lungs, and kidneys.
Diffuse scleroderma can present with a rapid progression of skin thickening within the first few years after onset. The skin involvement may extend to areas beyond the hands, feet, and face, which are commonly affected in limited scleroderma (another form of systemic sclerosis). Additionally, patients with diffuse scleroderma have a higher risk for severe internal organ complications compared to those with limited scleroderma.
Early diagnosis and appropriate management of diffuse scleroderma are crucial to prevent or slow down the progression of organ damage. Treatment typically involves a multidisciplinary approach, focusing on symptom management, immunosuppressive therapy, and addressing specific organ involvement.
Limited scleroderma, also known as limited cutaneous systemic sclerosis (lcSSc), is a subtype of scleroderma, a chronic autoimmune connective tissue disease. In this form, the fibrosis or hardening and thickening of the skin is generally limited to areas below the elbows and knees, as well as the face and neck.
The limited cutaneous form often involves the hands, causing a tightening of the skin on the fingers, known as "sclerodactyly." It can also affect the internal organs, but this is usually less severe and occurs later in the disease course compared to diffuse scleroderma.
A common characteristic of limited scleroderma is the presence of CREST syndrome, an acronym for Calcinosis, Raynaud's phenomenon, Esophageal dysmotility, Sclerodactyly, and Telangiectasia. These are specific symptoms associated with this subtype.
However, it is important to note that the manifestations of scleroderma can vary significantly from person to person, and not everyone with limited scleroderma will develop all the features of CREST syndrome.