Use LEFT and RIGHT arrow keys to navigate between flashcards;
Use UP and DOWN arrow keys to flip the card;
H to show hint;
A reads text to speech;
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
|
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
|
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) DR 4 RA 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 |
|
Graves
|
Type II hypersensitivity
damage to thyroid Rs |
|
Myasthenia Gravis
|
Type II hypersensitivity
damage to ACh Rs |
|
Goodpastures
|
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)
vasculitis |
|
Post-streptococcal glomerularnephritis
|
type III hypersensitivity
|
|
mechanism of damage & symptoms of Post-Strep glomerulonephritis
|
inflammation (complement & FcR)
nephritis |
|
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 Lyn, ITAM, MAPK Granule exocytosis |