Immunology 2 Flashcards
(27 cards)
Peripheral tolerance
additional mechanisms in periphery (OUTside bone marrow and thymus) that help ensure self-tolerance
ie: - require B7 for T cell activation
- require CD4 T cell for B cell activation
- T reg cell (regulation)
* *most Ags require CD4 T cells for B cell activation –> CD40(L)
Microglial cell
the resident macrophage of the CNS
Multiple sclerosis
T cell-mediated neurodegenerative disease (autoimmune issue)
–> demyelinate CNS neurons
(Ags targeted: myelin basic protein, proteolipid protein, myelin oligodendrocyte glycoprotein)
consequence: muscle weakness, blindness, paralysis
Treatment: prevent antibody migration (alpha4 integrin blocker or FTY720)
Rheumatoid arthritis
chronic autoimmune disease in synovium (joint linings);
CD4 T cells trigger cytokine release –> inflammation (esp. from INFa)
* treat w/ TNF inhibitors*
genetic: associated w/ certain MHC class II genes
Crohn’s Disease
autoimmune disease, = Inflammatory Bowel Disease;
CD4 T cells target GI commensal flora –> chronic inflammation
* genetic basis: loss of function mutations in NOD2 protein*
- maybe failure to regulate”DMZ”
* treat w/ Glucocorticoids, TNFa inhibitors, alpha4 integrin blocker
Autologous Graft
graft from one individual to different site on self
Syngeneic graft
graft between identical twins
Xenograft
graft from one species to another
ie: porcine heart valve to human
Graft vs. host disease
serious disease, immune cells in graft recognize and react to the host components
Rejection (of grafts)
destruction of graft organ or tissue,
mediated by antibodies and T cells of the host
autoimmunity
immune responses directed against self-antigen;
mediated by autoreactive B cells and antibodies, and/or T cells
- regulated/controlled by central tolerance and Tregs
Central tolerance
Main process for regulating autoimmunity,
–> delete self-specific B or T cells (in bone marrow or thymus)
Treg Cell
T cell w/ moderate affinity for self-Ag,
used to suppress reaction to self-Ags
* esp. w/ up-regulation of Fox3P
Anergy
perpetual non-proliferative state of T cell (no activation),
result of incomplete signals for activating T cells
(ie: only MHC or B7 but not both)
Role of CD4 cells in autoimmunity
- necessary for most autoimmunity responses *
- activate macrophages –> inflammation
- help auto-reactive B and CD4 cells
Mechanism of type I diabetes
autoreactive T cells selectively destroy beta cells of islets of Langerhans (which produce insulin);
* genetic factor: influenced be certain HLA II alleles*
Humoral autoimmunity
result of auto-antibodies against self; causes complement activation and chronic inflammation.
bind to…
- specific receptor molecs –> inhibit OR constantly activate the R!
- transmembrane proteins
* can form complexes w/ Ag that precipitate in diff. organs
Grave’s Disease
problem of auto-antibodies specific to TSH (thyroid-stimulating hormone) that ACTIVATE TSH receptors
- -> enlarged thyroid, etc.
treatment: surgery, radioiodine and anti-thyroid drugs
Myasthenia Gravis mech.
auto-antibody attack on nicotinic ACh receptors,
–> block transmission at NMJ ==> progressive weakness
Systemic lupus erythematosus (“SLE”)
disease: auto-antibodies against common cell parts (ie: DNA proteins); * similar to type III hypersensitivity,
- immune complexes from dying cells -> deposited on walls of blood vessels, etc. –> activate innate immune cells via Fc Rs –> more auto-Abs
Toll hypothesis
related to SLE (lupus),
–> auto-immunity (esp. w/ auto-Antibodies) may be triggered by under-methylated CpG segments, so appear microbial!
Type I hypersensitivity rxn
Immediate allergic rxn mediated by IgE,
reacts to…pollen, food, venom, drugs;
1st exposure: sensitization to the allergen (innocuous Ag)
2nd exposure: triggers mast cells, basophils, eosinophils on second exposure
Rxn to helminths
bc = too big for phagocytosis,
must elicit Th2 and IgE response
–> mast cells, basophils, eosinophils
Atopy
= predisposition to develop IgE responses to common environmental antigens –> develop many allergies.
- -w/ genetic and environmental factors –
env. factors: early life microbe exposure and commensal flora can predispose for Th1 response and high Treg activity