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Hypersensitivity
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What is hypersensitivity?
An exaggerated response to a typically harmless antigen that results in injury to the tissue, disease, or even death.
What is the Gell and Coombs Classification System?
A classification system that categorizes hypersensitivity reactions into four types: Type I, Type II, Type III, and Type IV.
What is Type I Hypersensitivity?
An immediate hypersensitivity reaction where exposure to an antigen induces the production of specific IgE antibodies, leading to degranulation of mast cells and basophils.
What is Type II Hypersensitivity?
An immediate hypersensitivity reaction where IgG or IgM antibodies react with antigens on host cells, leading to cell damage by complement-mediated lysis or other mechanisms.
What is Type III Hypersensitivity?
An immediate hypersensitivity reaction where IgG or IgM antibodies react with soluble antigens, forming small complexes that activate complement and cause an inflammatory response.
What is Type IV Hypersensitivity?
A delayed hypersensitivity reaction where sensitized T cells, rather than antibodies, are responsible for inducing inflammation and tissue damage.
What is the distinguishing feature of Type I Hypersensitivity?
A short time lag (usually minutes) between exposure to the allergen and the onset of clinical symptoms.
What is passive cutaneous anaphylaxis?
An experiment conducted by Carl Wilhelm Prausnitz and Heinz Kstner, where serum from patients with allergic hypersensitivity reactions was shown to produce a large amount of IgE antibody in response to a small concentration of allergen.
What are allergens in type I hypersensitivity?
Antigens that trigger type I hypersensitivity, such as peanuts, eggs, and pollen.
What is the distinguishing feature of type I hypersensitivity?
Short time lag, usually minutes, between exposure to allergen and onset of clinical symptoms.
Who provided the first clue about the cause of type I hypersensitivity?
Carl Wilhelm Prausnitz and Heinz Kstner.
What is passive cutaneous anaphylaxis?
Occurs when serum from an allergic individual is transferred to a non-allergic individual who is later challenged with the specific allergen, resulting in redness and swelling.
What does atopy refer to in type I hypersensitivity?
An inherited tendency to develop classic allergic responses to naturally occurring inhaled or ingested allergens.
What are the key immunologic components in type I hypersensitivity?
IgE antibody, mast cells, basophils, and eosinophils.
What initiates the transcription of the gene that codes for the epsilon heavy chain of immunoglobulin molecules in type I hypersensitivity?
IL-4 and IL-13, among other cytokines.
Autoimmunity
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What is horror autotoxicus?
Horror autotoxicus is a phenomenon observed by Paul Ehrlich where the immune system attacks the host it is meant to protect, leading to autoimmune diseases.
What are autoimmune diseases characterized by?
Autoimmune diseases are disorders in which immune responses target self-antigens, resulting in damage to organs and tissues in the body. This can be caused by T-cell-mediated immune responses or autoantibodies directed against host antigens.
What is self-tolerance in the context of the immune system?
Self-tolerance is the ability of the immune system to accept self-antigens and not initiate a response against them. It is a state of immune unresponsiveness directed against specific self-antigens.
What is central tolerance and where does it occur?
Central tolerance occurs in the thymus and bone marrow, the primary lymphoid organs. T cells mature in the thymus encounter self-antigens, and those with high affinity are deleted through negative selection by apoptosis.
What is peripheral tolerance and how is it achieved?
Peripheral tolerance refers to lymphocytes in secondary lymphoid organs being rendered incapable of reacting to self-antigens. This can occur through anergy from a lack of costimulatory signals, inhibition by Tregs or apoptosis.
How do self-reactive B cells in the bone marrow undergo tolerance mechanisms?
Self-reactive B cells in the bone marrow are eliminated through apoptosis if they recognize self-antigens strongly. Some are stimulated to rearrange their immunoglobulin genes to become non-antigen specific (receptor editing) or downregulate receptor expression (anergy).
Why are autoimmune diseases often more prevalent among family members and genetically identical twins?
Autoimmune diseases show higher prevalence among family members and monozygotic twins due to genetic factors. Examples include HLAB27 allele for ankylosing spondylitis, TPN22 gene, IL2RA gene, and CTLA4 gene.
How can B cells in the periphery be deleted?
B cells in the periphery can be deleted by apoptosis, rendered anergic after repeated stimulation with self-antigens, or receive inhibitory signals through receptors such as CD22.
What are some factors that contribute to the prevalence of autoimmune diseases among family members and twins?
Autoimmune diseases are more prevalent among family members and monozygotic twins than among unrelated individuals or dizygotic twins. Examples include HLAB27 allele, TPN22 gene, IL2RA gene, CTLA4 gene, and BLK gene.
How does hormonal influence affect the immune system in women?
Women are more likely to acquire autoimmune diseases than men. Estrogens tend to direct the immune system in favor of a Th2 response, leading to more B cell activation and antibody production. Androgens favor a Th1 response with activation of CD8 T cells.
What is immunologic ignorance and how can it lead to autoimmune responses?
Immunologic ignorance occurs when cryptic self-antigens are hidden within tissues and are later released due to inflammation or tissue trauma, triggering an immune response. This may be caused by factors like infections, environmental toxins, or physical injury.
What is molecular mimicry and how can it contribute to autoimmune disease development?
Molecular mimicry refers to microbes containing antigens that resemble self-antigens, leading to autoimmunity. For example, Streptococcus pyogenes in rheumatic fever. It is a principal means by which microbes trigger autoimmune diseases.
What are epigenetics and Modification of Self-Antigens?
Refers to modifications in gene expression that are not caused by changes in the original DNA sequence, stable, and can be inherited.
What triggers epigenetic changes?
Exposure to environmental toxins, ingestion of harmful foods or drugs, or the aging process can induce epigenetic changes by increasing or decreasing methylation of cytosine bases, modifying histones, and causing abnormal regulation by microRNAs.
What biochemical processes are involved in posttranslational modifications as a result of exposure to environmental factors?
Acetylation, lipidation, citrullination, and glycosylation may occur, where, for example, citrullination of collagen might play a role in rheumatoid arthritis (RA) pathogenesis and glycosylation of myelin may be involved in the pathology of multiple sclerosis.
Autoimmunity Maam Nicole
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What is autoimmunity?
Conditions wherein autoantibodies and autoreactive cells result in organ or tissue damage.
What is self tolerance in autoimmunity?
The ability to recognize own cell antigens and not react to self antigens.
What is central tolerance in autoimmunity?
Destruction of potentially self-reactive cells during maturation of T cells in the thymus and B cells in the bone marrow.
What is peripheral tolerance in autoimmunity?
Maintained by a balance between Th1 and Th2 cells, regulatory T cells, and T helper subsets in secondary lymphoid organs like lymph nodes and spleen.
Explain the balance between regulatory T cells and effector T cells in autoimmunity.
In a healthy individual, there is a balance between regulatory T cells and effector T cells. An imbalance can lead to autoimmune diseases due to an increase in effector T cells and inflammation production.
How does Major Histocompatibility Complex (MHC) influence autoimmunity?
MHC can influence autoimmunity through inheritance of specific MHC genes, expression of Class II molecules, and playing a vital role in self-tolerance.
What is tissue injury in the context of autoimmunity?
Exposure of antigens, usually not encountered by the circulation, due to trauma or infection can lead to autoimmune responses, such as the production of antibodies against self-antigens.
What is molecular mimicry in autoimmunity?
Molecular mimicry refers to similarities in the molecular structure between human/self antigens and viral/bacterial agents, which can trigger the production of antibodies with similar structures.
What is polyclonal B cell activation in autoimmunity?
Activation of two or three subsets of antibodies against different kinds of structures, leading to a more diverse immune response compared to monoclonal activation.
What triggers the production of antigens with similar molecular structures?
Exposure to antigens like Poliovirus VP2, Acetylcholine ACH, Measles Virus P3, Myelin Basic Protein, Papilloma Virus E2, Insulin Receptors
What are the possible defects that may include abnormalities in the immune system?
1. Abnormal expression or function of key signaling molecules 2. Dysregulation of cytokines 3. Changes in B cell development subsets
Which organisms can enhance immune system defects?
Gram negative bacteria, Cytomegalovirus, EBV (Epstein Barr virus)
How does EBV infection lead to immune system defects?
EBV infects B cells, causing their proliferation and overproduction of antibodies, leading to an imbalance in regulation and potential autoimmunity.
What are some other mechanisms of defects in the immune system?
Defects in natural killer cells surveillance, secretion of cytokines, apoptosis, and complementary components
What age group is usually affected by SLE?
20-40 years old
Scholarly Assistant's Insights
Learn about hypersensitivity reactions, Gell and Coombs Classification System, and different types of hypersensitivity.
Hypersensitivity Reactions
Immunology
Allergies
Clinical Manifestations
Skin Tests
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