Immunology Flashcards
IgM
- on naive B cells, expressed as receptor and soluble antibody
- produced early in B cell pathway, activates classical complement path
- receptor on naive B cells
IgG
- expressed on activated B memory cells that have class switched
- major type in blood, transfer across placenta
- activate classical complement pathway
- mediate neutralization and opsonization of pathogens
- mediate antibody dependent cellular cytotoxicity
IgA
- expressed on activated memory B cells that undergo class switching
- produced in mucosal tissue and secreted into lumens of GI and respiratory tract
- mediate pathogen neutralization
- transferred in breast milk
IgE
- expressed on active memory B cells that have class switched
- defense against helminths
- allergic responses
Th1 cells
- recruit monocytes
- IFN-gamma secretion
- host defense against intracellular microbes
- involved in inflammation
Th2 cells
- recruit eosinophils
- IL4,IL5,IL13 secretion
- host defense against helminths
- allergic reactions
Th3 cells
- recruit neutrophils and monocytes
- IL17 secretion
- host defense against bacteria and fungi
- inflammatory disorders
T Follicular Helper cells (Tfh)
- produce IL21, IL4
- express CD40 and ICOS to help B cells proliferate and make high affinity, class switched antibodies
T regulator cell (Treg)
-inhibit immune responses via cell surface molecules of cytokines such as IL10
Interleukin 2
- made by T cells
- T cells: proliferation, increased cytokines synthesis, potentiates Fas-mediated apoptosis, promotes Treg development, survival
- NK cells: proliferation, activation
- B cells: proliferation, antibody synthesis (in vitro)
Interleukin 4
- Source: CD4+ T cells (Th2), mast cells
- B cells: Isotype switching to IgE
- T cells: Th2 differentiation, proliferation
- Macrophages: inhibition of IFN-gamma mediated activation
- Mast cells: proliferation (in vitro)
Interleukin 10
- inhibitor of cytokines
- anti-inflammatory
- produced by monocytes, Th2, mast cells, Tregs
Interleukin 8
- Chemokine that recruits neutrophils (CXCL8)
- produced by macrophages, epithelial cells, endothelial cells
Interferon-gamma
- source: T cells (Th1,CD8+ T cells), NK cells
- B cells: isotype switching to opsonizing and complement fixing IgG subclasses
- T cells: Th1 differentiation
- macrophages: activation (increased microbicidal function)
- various cells: increased expression of class I and class II MHC, increased antigen processing and presentation to T cells
Interleukin 17
- source: T cells
- endothelial cells: increased chemokine production
- macrophages: increased chemokine and cytokines production
- epithelial cells: GM-CSF and G-CSF production
TGF-beta (transforming growth factor)
- source: T cells, macrophages, other cell types
- B cells: inhibit proliferation, IgA production
- T cells: inhibit proliferation and effector functions
- Macrophages: inhibit activation, stimulate angiogenic factors
- fibroblasts: increased collagen synthesis
Central tolerance for B-cells occurs in the… and use which to mechanisms?
- bone marrow
- negative selection (actively killing)
- receptor editing of the light chain in Ab
How does peripheral b-cell tolerance occur in…
1) presence of t-cells
2) absence of t-cells
1) actively killed during clonal expansion via Fas-FasL mediated AICD, Fc receptor inhibition
2) decreased BCR expression leads to anergy of b-cell, decreased CXCR5 leaves to exclusion from lymphoid follicule
T-cell central tolerance takes place in the…
thymus
T-cell positive selection is…
when T-cell maturation occurs with binding to self-peptide and MHC determines CD4 or CD8
Negative selection of T-cells
immature t-cells
that encounter high affinity self-peptide and MHC are actively killed (negative selection) and/or develop into natural Treg cells to suppress other T effector functions
AIRE
This protein modulates interaction of self-peptide with MHC and it’s presentation to T-cells during central tolerance
Plays a role in preventing autoimmunity
What are two ways that infection can lead to auto-reactivity?
1) Activation of APC that are presenting self-antigen already (as cryptic epitopes) are activated by the pathogen –> causes expression of costimulatory molecules –> self-reactive T-cell activation
2) Microbe may use the method of molecular mimicry which presents self-antigen like antigen to self-reactive t-cell –> activation –> autoimmunity
Activation of
What are two mechanisms by which auto-immunity can progress?
1) Amplification of response by release of cytokines –> an increase in self-reactive clones number
2) Spreading of the epitope due to tissue injury –> more antigens presented –> more diverse self-reactive t-cells made
