Exam #3 Flashcards
(31 cards)
Vladimir Badovinac & John Harty
Death of effector T cells is independant of clearance of infection
Sue Kaech & Rafi Ahmed
Memory Cells are present during effector phase of T cell response and can be definied by expression of IL–7R chain
Joe Sun & Mike Bevan
CD8 T cells that are primed without CD4 T cells don’t have memory. Possible mechanism is that these cells have proliferated more and have then died?
Th1 Cells
Intracellular pathogens, Macrophages,
cytokines affecting differentiation IL-12 & IFN-g,
STAT pathway is STAT1 (IL-12) and STAT4 (IFN-g),
Transcription factor is T-bet,
Cytokines produced by CD4 helper cell: IFN-g
B cell isotypes induced: IgGa, IgG3
Beneficial effects: Macrophage activation, clearence of intracellular pathogens
Harmful effects: Systemic pathology
Th2 Cells
Extracellular parasites Eosinophils, basophils, mast cells Cytokines affecting differentiation: IL-4 STAT pathwy: STAT6 Transcription factor: GATA3 Cytokines produced: IL-4, IL-5, IL-13, B cell isotypes induced: IgE, IgG1 Beneficial effects: Eosinophil, basophil, and mast cell activation, clearence of extracellular pathogens, Harmful effects: Allergies and asthma
Th17
Extracellular bacteria/fungi
Neutrophils
Cytokines affecting differentiation: IL-6, IL-23
STAT pathway: STAT3
Transcription factor RORgt
Cytokines produced: IL-17, IL-6
B cell isotypes induced: IgA, IgG2b
Benefits: Neutrophil activation, clearence of extracellular bacteria/fungi
Harful effects: Autoimmunity and Inflamation
Treg
Activated by ongoing immune response Cytokines affecting differentiaion: IL-2 STAT pathway +: STAT5 Transcription factor: FOXP3 Cytokines produced: IL-10, TGF-b Does not induce B cell isotypes Inhibits overaction of other T cells
What are the 3 ways AID induced mutation can be repaired?
- Replication –> GC pair and AT pair
- Repair using MSH2/6 –> GC and mutates nearby AT segments
- Cleavage by UNG to abasic site and repair of abasic site by REV1 –> Cleave U and replaces with a random base
IFNy
Produced in response to systemic infection, signals through STAT1, induces Igy S-transcripts and IgG. Results in systemic antibodies
TGFb
Produced in response to T cells in mucosal lymphoid tissue, signals through smad 2/3, induces Iga S-transcripts and IgA. Results in mucosal antibodies
IL-4
Produced in response to pathogens at epithelial surface, signals through STAT3/6, Induces Ige S transcripts IgE, Allows mast cells to enhance immunity at epithelial surfaces
Name 4 routes for antigen to be taken up for presentation to T cells
- receptor mediated phagocytosis (LN resident DC)
- macro-pinocytosis (LN resident DC)
- viral infection (any DC)
- Cross presentation after phagocytic or macropinocytic uptake (dv103+ DC)
CD103+ DC
Migratory DC that is good at Ag cross-presenting and starting a T cell response
Plasmacytoid
LN Resident DC that is the main source of Type I IFN
IgM
antibody whose main function is complement activation and initial killing of microbes
IgG
Main serum antibody ( 4 subtypes) main function is neutralization, opsonization for phagocytosis, NK cell activation via Fc receptors, complement activation
IgA
Main mucosal antibody (2 subtypes) Main function if neutralization in mucosa
IgE
Epithelial surface antibody that binds to Fc receptors on mast cells and basophils
FRN
Follicular Reticular Network in LN that free Ag ride in, T cells and DC cells travel on, ect
Transcytosis
The process of going through a macrophage to another side
AID
Acivation Induced Deaminase. Triggered by CD40 signalling adn converts C to U.
CD40 signalling
B cells activated by agiC3b or BCR crosslinking upregulate CD40. T cells activated by DC express CD40L and migrate to B zone. Signalling gets full activation for both T and B cells.
WIthout this B cell forms primary foci for short lived IgM response
Cross-linking
T cell independant. Cross-linking of BCR and CR2. Occurs due to multipble Ags and iC3b on microbial surfaces or FDC
What are the steps for a lymphocyte to enter the LN via HEV
Rolling: Selectins such as L-selectin (aka CD62L)
Activation: Chemokines such as CCL21
Adhesion (makes high affinity): Integrins suchas LFA-1
Diapedesis: chemokines such as CL21 and CXL12