Chapter 6: Diseases of the immune system Flashcards
Name the main constituents of the innate immune response:
1) Epithelial barrier
2) Phagocytic cells (macrophages neutrophils)
3) NK cells
4) Complement
5) Dendritic cells
How does TLRs work?
1) Binds PAMP
2) Through NF-kappa-B activates the cll to secrete cytokines which recruits leukocytes.
Main reactions of innate immunity:
1) Inflammation - cytokines and complement
2) antiviral - Interferon type I acts on cells and activates enzymes that degrade viral nucelic acids.
NLRs?
Nod like receptors - activates inflammasome which cleaves IL-1 and makes it acctive - pro inflammatory.
Main constituents of the adaptive immune response:
1) Lymphocytes and their secreted proteins
Humoral immunity:
Adaptive branch - extracellular microbes defense. - mediated by B-cells and antigens
Cell mediated immunity?
Adaptive branch - intracellular immunity - mediated by T-cells
Innate cytokines:
TNF, IL-1, IL-12, Type I interferons, IFN-gamma.
Adaptive cytokines:
IL-2, IL-4, IL-5, IL-17
Immune surpressive cytokines:
IL-19 and TGF-Beta
Colony stimulating cytokines:
CSF (GM-CSF in particular granulocyt macrophage) and IL-7.
What is hypersensitivity?
A harmful immune reaction to a given antigen.
1) can be elictid by self or non-self antigens
2) Usually imbalance between effector mechanisms and control mechanisms.
Hypersensitivity classification:
Type I = Immediate (Th2, IgE and Mast cells)
Type 2 = Antybody mediated
Type 3 = Immune complexes
Type 4 = cell mediated
Type I sensitivity pathogenesis:
1) exposure to antigen and bynding by APC
2) APC show to T-cell - differentiate into Th2
3) IL-4 (IgE switch 0 more th2), IL-5 (eosinophiles) and IL-13 (enhances IgE prod.) is produced and T
Mediators within mast cell granules:
1) vasoactive amines - eg histamine
2) Enzymes - proteases
3) Proteoglycans - eg heparin (anticoagulant)
4) Arachnoid acid derivviates - eg prostaglandins, leukotrienes, platelet activating factor
5) cytokines - IL-1, TNF, IL-4,
What is late phase reaction?
In the type 1 response it is induction of chronic inflammation by eosinphile granulocytes.
Type II hypersensitivity:
1) antibodies on cells
2) activates complement
3) complement C3a etc leads to recruitment of leukocytes and increase in vascular permability.
4) leukocytes activated by complement and AB.
Type III hypersensitivity:
1) Formation of immune complexes by binding of many antibodies to the same antigen. (both exogenous and endogenous antigens)
2) Depositions of immune complexes in the vessel walls.
3) inflammation
Type IV hypersensitivity:
1) APC shows antigen to CD4 T-cell - T-cell differentiates into Th1 or Th17 Subset.
2) T-cell secretes cytokines
3) cytokines are pro-inflammatory.
Mechanisms of autoimmunity:
1) defective tolerance or regulation
2) Abnormal display of self antigens
3) Inflammation or initial innate immune response
