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96 Cards in this Set
- Front
- Back
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anaphylatoxins
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induce an inflammatory response by stimulating the release of histamine from mast cells - ex C3a, C4a, and C5a released during complement fixation
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antigenic determinant (epitope)
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site on antigen that binds to the hypervariable regions on light and heavy chains of the immunoglobulin
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autoimmune disease
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breakdown of immunological tolerance
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c3b
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active fragment of complement component - can coat foreign particles (opsonization) thereby enhancing phagocytosis by cells which possess receptors for C3b
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HIV
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infects helper T lymphocytes by binding to the CD4 molecule
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class switching
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B lymphocyte alters the class of immunoglobulin - determined by structure of heavy chain constant region - by deletion of DNA gene segemnts or differential splicing of RNA.... signals which drive class swtiching are delivered by various ILs secreted by T cells
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classical complement
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IgM, IgG1, IgG2, IgG3 after binding antigen, activate the first component int he classical pathway
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histamine
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anaphylatoxins and antigen-crosslinked IgE stimulate the release of histamine from mast cells
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IgA
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in the external secretions: gut, lungs, eyes, mouth and GI, also present in breast milk
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IgD
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minor class in glood - present on the surface of B lymphocytes during differentiation
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IgE
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bound to the surface of mast cells and basophils by a high affinity IgE receptor
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IgG
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can cross the placenta
IgG1, IgG2, IgG3 can fix complement main immunoglobulin produced during a secondary response |
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IgM
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first class to evolve, first to be produced during a primary response
can bind up to ten antigenic determinants - can efficiently agglutinate microorganisms and fix complement |
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active immunizatoiin
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administration of antigen - generating a primary response
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passive immunization
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administration of antibody to confer temporary protection
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interferons
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proteins that interfere with virus replication
alpha and beta are important in innate immunity gamma acts as a lymphokine, increasing the killing activity of cytotoxic T cells, macrophages, monocytes, and neutrophils |
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interleukins
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growth and differentiation factors
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J chain
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found in immunoglobulin molecules - induces polymerization by means of disulfide bonds
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lymphokines
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growth and differentiation factors produced by antigen-stimulated lymphocytes which act on various cells, including lymphocytes, macrophages, monocytes and neutrophils
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monoclonal antibody
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homogenous antibody produced by a clone of identical B lymphocytes that only recognizes a single antigenic determinant
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monocytes
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attracted to the site of infection (ex by the C5a fragment of complement) where they ingest particles or microorganisms by phagocytosis - enhanges if the particle has been coated by C3b or antibody (opsonization)
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T-independent antigens
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usually large, repeticve structures such as polysaccharides of bacterial cell walls can stimulate the production of antibody in absence of T helper
the immune response is usually restricted to IgM antibodies |
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TCR
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closely associated with the CD3 moleucles expressed on T lymphocytes and normally only recognizes antigen in association with MHC proteins
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T regulatory lymphocytes
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subpopulation involved in regulating the antibody response and cell mediated immnity - express FOX3, CD4, and CD25
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tolerance
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the development of antigen-specific NON-reactivity of lymphocytes to an antigen normally capable of sitmulating an antibody response
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TLR2
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bind parts of gram postive bacteria, on macrophages, DCs, neutrophils
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TLR4
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bind parts of gram negative bacteria, on macrophages, DCs, neutrophils, on B cells
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TLR5
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bind flagellin, on macrophages, neutrophils
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TLR9
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binds unmethlyated CpG, on macrophages, neutrophils
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CR3, CR4
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Complement receptor, facilitates phagocytosis
on macrophages, neutrophils |
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Fc receptors
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specific receptors for isotopes of IgG, facilitates phagocytosis
on macrophages, DCs, neutrophils, NK cells |
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IL-1
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inflammation and fecer, activates vascular endothelium, lymphocytes, phagocytes, APC, acute phase response
released by macrophages, endothelial cells |
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IL-6
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activates lymphocytes, antibody production, acute phase response from the liver, induces fever
released by macrophages |
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CXCL8
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chemokine - factor for leukocytes, neutrophils
released by macrophages |
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IL-12
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activates NK cells, promotes Th1 differentiation
released by macrophages |
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TNF-alpha
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increases vascular permeability, facilitates shock, cell death, fever -> sepsis
released by macrophages and T cells |
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CD80, CD85
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accessory molecule that binds CD28 for costimulation of naive T cells
on macrophages, DCs |
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follicular dendritic cells
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want to retain antigen - use Fc receptors, complement receptors
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Fc receptor for IgE
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binds IgE, release of histamine containing granules during hypersensitivity
on eosinophils, basophils, mast cells |
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CD94:NKG2
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inhibitory receptor recognizes HLA-E, on NK cells
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Killer cell Ig-like receptors KIRS
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inhibotory receptor recognizes HLA-E, HLA-B, HLA-c
on NK cells |
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IFN-gamma
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activates macrophages, APCs, increases MHC expression, inhibit Th2
NK cells are activated by IL-12, TNF-alpha, IFN alpha/beta - activating them to secrete IFN-gamma leads to class switching to IgG also produced by Th1 |
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CD28
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binds CD80/CD86 on B cells
on CTLs |
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IL-2
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aids in proliferation of lymphocytes, NK cells, autocrine or paracrine
produced by T cells or NK cells |
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CD40L
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binds CD40 on B cells
on T cells |
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IL-3
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induces macrophages and granulocytes in bone marrow, growth of hematopoietic progenitors- produced by Th1
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GM-CSF
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induces macrophages and granulocytes in bone marrow - produced by Th1
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IL-4
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B cell proliferation, increase in MHC class II on B cells, aids in activation of eosinophils, mast cells
activation and isotype switching to IgE to fight helminths - produced by Th2 |
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IL-5
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aids in eosinphil acitvation - produced by Th2
promotes class switching to IgA |
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IL-6
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aids in antibody production - produced in Th2
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IL-10
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inhibits Th1, NK; suppresses cellular response (downregulates macrophages), aids B cells and antibody response
produced in Th2 |
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TGF-beta
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anti-inflammatory, inhibits macrophage cytokine production and MHC class II, prevents Th1- produced by Th2
promotes class switching to IgA |
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CD45RA
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marks naive T cells
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LFA-1
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binds ICAM1, ICAM2
on T cells |
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FasL
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on activated CD8 cells - binds Fas on target cells to induce apoptosis
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CD25
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component of IL-2 receptor (on immature thymocytes)
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FOXP3
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cell surface marker on T regulatory cells
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IFN-alpha/beta
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indces antiviral effects in neighboring cell tot contorl early viral replication and infection, activates NK cells, macrophages, increase MHC class I
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G6PD deficiency
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impaired respiratory burst
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Chronic granulomatous disease
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loss of component of NADPH oxidase - impaired respiratory burst
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myeloperoxidase deficiency
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failure to form hypocholorite ions and downstream reactive species
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Chediak-Higashi Syndome
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defect in granule transport, impaired killing of phagocytosed pathogen
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hereditary angioneurotic edema
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C1 inhibitor
edema from excess anaphylatoxin generation |
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Factor I deficiency
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little intact C3; susceptible to ear infections
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C3 deficiency
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susceptibility to encapsulated bacteria
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C5-C9 defiencies
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no MAC; susceptibility to Neisseria infections
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paroxysmal nocturnal hemoglobinuria
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DAF deficiency; hemolysis - MAC forms on erythrocytes
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Hyper IgM syndrome
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CD40/CD40L, activation induced cytidine deaminase, uracil nucleotide glycosylase -- inability to class switch (CD40L gene is X linked) - need T cell activation to class switch
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Agammaglobulinemia
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arrest of B cell decelopent at pre-B; most are x-linked (Brutun's defect in BTK) --> produce identical phenotypes
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IgA deficiency
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asymptomatic
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CVID (common variable)
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recurrent infections with hypogammagloculinemia - reduced serum IgG, IgA, or IgM - absent responses to previous vaccines
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Specific Antibody Deficiency
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normal IgG, IgA, IgM, normal T, normal T, normal vaccine response
deficiency in TI-2 B cell pathwya impaired response to polysaccharides (and thus encapsulated bacteria) |
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Transient Hypogammaglobulinemia of Infancy
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Low IgG with normal specific antibodies - recurrent sinopulmonary infections, resolves by age 4
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C1, C2, or C4 deficiency
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autoimmune iseases and increased susceptibility to infection
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SCID
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profound decrease of B, T, and NK cells
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adenosine deaminase deficiency
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general lymphopenia, acumulation of deoxyATP
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various IL receptor deficiencies
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T-, B+, NK-; X-linked inheritance
If no IL-7, no T cells |
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IL-7
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from bone marrow stromacl cells - induces growth of lymphocytes
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Jak3 deficiency
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T-, B+, NK-
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RAG (recombination activation gene) deficiency
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used in the generation of BCR and TCR
T-, B-, NK+ |
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CD3 deficiency
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T-, B+, NK+
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wiskott aldrich syndrome
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WA protein deficiency --> eczema, thrombocytopenia, and immmune deficiency
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DiGeorge syndrome
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failure of development of the 3rd and 4th pharyngeal pouches --> defects in parathyroids, aortic arch, heart, face and thymus
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autoimmune polyglandular syndrome Type 1 - APS1
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defective autoimmune regulator gene (AIRE) - faulty expression of antigens on medullary thymic epithelia
hypoparathyroidism, adrenal insufficiency, candida infections, organ-specific autoimmuniies, failure to maintain tolerance |
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IPEX
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FOXP3 deficiency leading to failure of regulatory T cell decelopment - leads to a failure of CD4CD25 regulatory T cell decelopment --> type 1 diabetes, autoimmune enteropathy, eczema, food allergies
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ALPS autoimmune lymphoproliferative syndrome
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various deficits in antigen-induced apoptosis --> chronic non-malignant lymphdenopathy + splenomegaly, increased susceptibilty to lymphoma in 10% of patients, autoimmune diseases
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Hyper IgE (Job syndrome)
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STAT3 signaling impaired, neutrophilic inflammation - recurrent cold abcesses, sinopulmonary infections, severe eczema
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leukocyte adhesion deficiency
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no neutrophil surface glycoproteins important in cell migration - recurrent soft tissue infections, delayed umbilical cord separation, no pus formation
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anaphylaxis
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TYPE I - IgE-mediated
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Acute rheumatic fever
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TYPE II - streptococcal cell wall antibodies cross react with mycardia antigens --> myocarditis, arthritis
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Graves disease
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TYPE II - antibodies produces to TSH recepotrs leads to hyperstimualtion - hyperthyroidism
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autoimmune hemolytic anemia
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TYPE II - opsonization of erythrocytes --> anemia
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myasthenia gravis
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TYPE II - Ach receptor (antibody inhibits binding) --> muscle weakness
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systemic lupus erythratosis
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TYPE III - antibodies --> DNA, nuclear proteins --> nephritis, arthritis, vasculitis
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serum sickness
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TYPE III - reaction to proteins in antiserum derived from a non-human animal source
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poison ivy, contact dermatitis, insulin dependent DM, MS
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TYPE IV - T cell mediated injury
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