Basic Immunology review Flashcards
3 cardinal features of acute inflammation
alterations in vasculature, structural changes in microvasculature, emigration of leukocytes to the site of injury
Features of chronic inflammation
active inflammation plus tissue destruction and repair. Autoimmunity is a major cause. See macrophages and lymphocyte predominance
Type I hypersensitivity: immune reactant, antigen, effector mechanis, example
IgE, soluable antigen, mast cell activation, allergic rhinitis, asthma, systemic anaphylaxis.
In words: free antigen binds to IgE on presensitized mast cells causing release of preformed histamine. There is an initial fast rxn (due to release of preformed mediators); delayed response is due to production of arachidonic acid metabolites.
Type II hypersensitivity: immune reactant, antigen, effector mechanis, example
IgG (or IgM). antigen: cell or matrix associated antigen causes complement and phagocytes and NK cells to attack. Example: some drug hypersensitivities, like penicillin
Or, Cell surface receptors. Effector mechanis is antibody altering signaling. seen in chronic uticaria
Type III hypersensitivity Rxn: immune reactant, antigen, effector mechanis, example
reactant: IgG, soluable antigen, causes complement and phagocytosis. Seen in serum sickness (immune complex formation and deposition that fixes complement and causes tissue damage) and Arthus rxn (ab-ag complexes in the skin).
Type IV hypersensitivity: immune reactant, antigen, effector mechanis, example
Immune reactants are Th1, Th2, and CTL cells.
Th1 cells: soluble antigen, macrophage activation, contact dermatitis
Th2 cells: soluble antigen, eosinophil activation, chronic asthma and chronic allergic rhinits
CTL: cell-associated antigen, causes cytotoxicityk, contact dermatitis
Basic features of innate immunity: what does it recognize, time scale, cells/mechanisms, memory?
fixed microbial antigen patterns called PAMPs; fixed receptors, fast response (minutes), occurs first, uses macrophages, PMNs, mast cells and complement. no memory
Adaptive immunity: what does it recognize, time scale, cells/mechanisms, memory?
universe of variable antigens, diverse receptors, slow response, T and B lymphocytes, has memory
What help contributes to self-tolerance?
requirement of B cells for T cell help
requirement for costimulation in naive T cell cell activation
negative selection in the thymus and bone marrow
lack of lymphocyte access to some tissues
restriction of MHCII to a few professional cells
suppression of autoimmunity by regulatory T cells
induction of anergy in autoreactive B and T cells
Mechanisms for loss of self-tolerance
immunization with autoantigen
exposure to cross-reactive antigens
lack of normal regulation/suppression
How to B cells depend on T cells?
B cells bind soluable antigens, take them up, and then present the antigens to T cells. In order for a T cell to bind the B cell, it too must recognize part of the antigen. Then, the T cell’s CD40 ligand will stimulate the B cell CD40 receptor. Both signals of T cell support are needed for B cells to be activated.
How do T cells recognize antigen? Describe T cell activation.
in the context of MHC complexes.
MHC class I is present on all cells except RBCs. It is recgonized by CD8 positive cells (2 CD8 molecs per cell). MHC class I presentsendogenous synthesized antigens. genetic loci are HLA-A, HLA-B, and HLA-C.
MHC class II is present on professional antigen presenting cells. It is recognized by CD4 positive cells (one CD4 molec with 2 subunits). Loci are on HLA-DR, LHA-DP and HLA DQ.
T cells need a second signal (ex. stim of CD28)- signal 1 w/o signal 2 = T cell anergy
If a diseases is MHC linked, T cells must play some role.
What are the genetic associations with rheumatoid arthritis?
an inflammatory arthritis associated with MHC II (HLA DR4). We think this arthritis involves a molecular mimicry phenomenon on the T cell side: pathogen peptides cause T cell activation, but there are self-peptide mimics in the same HLA that are also targeted by activated T cells. Type II collagen may be that mimic peptide.
(There are 4 walls in a rheum)
spondyloarthropathies: genetic associations
associated with MHC I (HLA B27)
Th1 cells: secretion, function, inhibition. What do they bind?
Th1: secretes IFN-gamma. activate macrophages and cytotoxic T cells. Inhibited by IL-4 and IL10 from Th2 cells. macrophages release IL-12 to stimulate T cells to differentiate into Th1 cells- and Th1 cells stimulate macrophages via IFN-gamma.
binds MHC II on antigen presenting cells.
