I&I hypersensitivity diseases
Terms
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- receptor editing
- B cell can make new receptor if 1st one doesn't function well for central tolerance
- 3 processes for peripheral tolerance
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anergy
deletion- activated by repetitive antigenic stim
immune suppression- T regulatory b/c T+self Ag- will suppress other self reactive - mechanisms to activate self reactive lymphocytes
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break T cell anergy- b/c microbe stimulates
molecular mimicry
injury to immune priviledged site - HLA genes involved in disease
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DR 2 & 3 is SLE
DR 3 & 4 DM (sugar no more)
DR 4 RA
B27 ankylosing spondylitis - Type I Hypersensitivity
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IL-4 cause switch to IgE (activate masts)
mast cell mediators (heparin & histimine)
inflammation (eos & basos) - Type II Hypersensitivity
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AB to cell or tissue antigen
IgM or IgG to self
Complement & Fc R mediate damage due to PMNs & MPs
May affect hormone receptors - Graves
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Type II hypersensitivity
damage to thyroid Rs - Myasthenia Gravis
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Type II hypersensitivity
damage to ACh Rs - Goodpastures
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Type II hypersensitivity
Ab to type IV collagen - Rheumatic fever
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Type II hypersensitivity
Ab to heart tissue - Autoimmune Hemolytic Anemia
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Type II hypersensitivity
opsonization of RBC
Antigen is Rh protein - Autoimmune Thrombocytopenia Purpura
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Type II hypersensitivity
opsonization of platelets
antigen is plt membrane protein - Pemphigus Vulgaris
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Type II hypersensitivity
antigen is epidermal cadherin
causes skin vesicles (bullae) - Pernicious Anemia
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Type II hypersensivity
damage to intrinsic factor of parietal cells
can't absorb B 12
abnormal EPoisis - Type III Hypersensitivity
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Circulating Immune Complexes
IgG & IgM
complement & recruitment of leukocytes - SLE- type of hypersensitivity
- Type III Hypersensitivity
- antigen in SLE
- DNA, Chromatin, Ribonuc prots, cellular constituents
- mechanism of damage in SLE & symptoms
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Mechanism of damage- inflamm (complement & FcR)
Symptoms- nephritis, arthritis, vasculitis - Polyarteritis nodosa
- Type III hypersensitivity
- antigen in Polyarteritis Nodosa
- Hep B or C surface Ag (from persistant infection)
- mechanism & symptoms of Polyarteritis Nodosa
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inflammation (complement & FcR)
vasculitis - Post-streptococcal glomerularnephritis
- type III hypersensitivity
- mechanism of damage & symptoms of Post-Strep glomerulonephritis
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inflammation (complement & FcR)
nephritis - Type IV Hypersensitivity
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delayed, cell mediated (Ts)
CD4 reacts to cell tissue Ag
Th1 activation (IL-12)
Activation of MPs (IFN) or CD8s bind directly to self - examples of Type IV hypersensitivity
- PPD, Poison Ivy,
- cytokine that activates Eosinophils
- IL 5
- Preformed mediators from mast cells
- histamine, heparin, tryptase
- new lipid synthesis in activated mast cell
- PLA2 (leads to PAF), PG, LT
- De Novo gene expression in activated mast cell
- cytokines (TNF, IL1, 3, 4, 13), GM-CSF, MIP-1
- Activation of Mast cells
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must be multi-valent antigen
binds 2 IgE on sensitized mast cell
Lyn, ITAM, MAPK
Granule exocytosis