Immunity Flashcards
People with a genetic deficiency in late components are at a higher risk for Neisseria meningitidis. What process is most crucial against the defense of N. meningitidis?
Formation of the membrane attack complex (MAC) for microbe lysis.
Gram negative infection from E. coli can activate what complement to start the classical pathway?
C1 complement can bind the E. coli endotoxin to activate the classical pathway.
Define Bare Lymphocyte Syndrome.
A condition where there are no MHC II proteins and therefore a direct inhibition of antigen presentations to Th cells (CD4). This mitigates cell-mediated immunity.
What cytokines do Th2 cells secrete?
Anti-inflammatory cytokines involved in Humoral immunity and allergies (acute hypersensitivity). These include:
IL-4: stimulates degranulation of mast-cells
IL-5: activates eosinophils
IL-13: activates macrophages
What cytokines do TH1 cell secrete?
Pro-inflammatory cytokines involved in cellular immunity and chronic infections (delayed-type hypersensitivity). These include:
IFN-gamma: activates macrophage killing capacity of ICF microbes
IL-2: T-cell growth and proliferation
What cytokines do Th17 cells produce?
Cytokines involved in neutrophilic and monocytic inflammation to fight ECF bacteria and fungi.
IL-17A: activate monocytes in the inflammatory process
IL-22: activates innate immune responses in epithelial cells (gut and respiratory tract)
What 3 major roles do complements play in inflammation?
Recruit phagocytes, microbial lysis (via MAC complex) and make it easier for macrophages to phagocytose coated microbes.
What is the function of Natural Killer (NK) cells?
NK cells target pathogens or unhealthy cells. They are extracellular killers that use performing, defensive and proteases to cause apoptosis of infected cells or lysis of microbes. Release IFN-gamma to activate macrophages.
What occurs in germinal center reactions?
B-cell activation for BCRs with higher affinity and class-switching recombination to IgG isotype. This mediates protection at the second exposure some time after immunization.
Loss of what transcription factor in T-regs results in an autoimmune disease? Explain the significance of this.
Loss of FOXP3 transcription factor can result in IPEX autoimmune disease because T-cells are not regulated or inactivated. This can manifest as DM I, diarrhea, dermatitis and can kill children within the first 2 years of life.
Compare and contrast central tolerance from peripheral tolerance.
Central tolerance involves + and - selection to which self-reactive T-cells can be turned into T-regs or killed at the thymus. Peripheral tolerance results in apoptosis, anergy or regulation of escaped, self-reactive T-cells.
Cells that lack what type of presenting peptide cannot go through positive selection?
Lack of MHC 1 and MHC 2 prevents a T-cell from going through positive selection in central tolerance. This is because only cells that bind to some MHC molecules survive.
What is the significance of the AIRE gene pertaining to autoimmunity?
Autoimmune regulator gene drives the expression of tissue specific antigen encoding genes. It’s due to this gene that epithelial-reticular cells of the thymus enable this organ to express all types of protein antigens. Lack of AIRE results in autoimmunity (DM I, Addison’s disease and yeast infections).
Describe the 2 ways in which a prolonged infection can cause autoimmunity.
- Molecular mimicry in which an antigenic protein that looks like a naturally-occuring protein in our body can cross-react leading to AI (i.e. Strept B and endocarditis).
- By-stander activation: killing of infection can cause collateral damage due to infiltration and a damaged self-protein can be mistaken as an antigen.
Explain how nature vs. nurture argument can be applied to the dev’t of autoimmunity.
Certain HLA subtypes (related to genetics) and an environmental trigger can increase the likelihood of developing an autoimmunity. (i.e. DR1 and DR4 at higher risk of developing DM I).
