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30 Cards in this Set

  • Front
  • Back
receptor editing
B cell can make new receptor if 1st one doesn't function well for central tolerance
3 processes for peripheral tolerance
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
break T cell anergy- b/c microbe stimulates
molecular mimicry
injury to immune priviledged site
HLA genes involved in disease
DR 2 & 3 is SLE
DR 3 & 4 DM (sugar no more)
B27 ankylosing spondylitis
Type I Hypersensitivity
IL-4 cause switch to IgE (activate masts)
mast cell mediators (heparin & histimine)
inflammation (eos & basos)
Type II Hypersensitivity
AB to cell or tissue antigen
IgM or IgG to self
Complement & Fc R mediate damage due to PMNs & MPs
May affect hormone receptors
Type II hypersensitivity
damage to thyroid Rs
Myasthenia Gravis
Type II hypersensitivity
damage to ACh Rs
Type II hypersensitivity
Ab to type IV collagen
Rheumatic fever
Type II hypersensitivity
Ab to heart tissue
Autoimmune Hemolytic Anemia
Type II hypersensitivity
opsonization of RBC
Antigen is Rh protein
Autoimmune Thrombocytopenia Purpura
Type II hypersensitivity
opsonization of platelets
antigen is plt membrane protein
Pemphigus Vulgaris
Type II hypersensitivity
antigen is epidermal cadherin
causes skin vesicles (bullae)
Pernicious Anemia
Type II hypersensivity
damage to intrinsic factor of parietal cells
can't absorb B 12
abnormal EPoisis
Type III Hypersensitivity
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
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
inflammation (complement & FcR)
Post-streptococcal glomerularnephritis
type III hypersensitivity
mechanism of damage & symptoms of Post-Strep glomerulonephritis
inflammation (complement & FcR)
Type IV Hypersensitivity
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
must be multi-valent antigen
binds 2 IgE on sensitized mast cell
Granule exocytosis