10.9 T and B cells Flashcards
_ cells are responsible for neutralization of microbes, phagocytosis, and complement activation
B cells are responsible for neutralization of microbes, phagocytosis, and complement activation
_ cells are needed for effective innate and adaptive immunity; they activate macrophages, increase inflammation, and cause proliferation/differentiation of T and B lymphocytes
Helper T cells are needed for effective innate and adaptive immunity; they activate macrophages, increase inflammation, and cause proliferation/differentiation of T and B lymphocytes
CD8+ cells directly kill infected cells by release of _ and _
CD8+ cells directly kill infected cells by release of perforin and granzyme
_ cells (of adaptive immunity) help to suppress the immune response
Treg cells (of adaptive immunity) help to suppress the immune response
B cells can float around and find antigen; however, T cells must be presented with antigen on _
B cells can float around and find antigen; however, T cells must be presented with antigen on MHC (in the form of small peptides)
* Antibodies can be secreted and travel in bloodstream
* T cells must always have constant region in the membrane
The TCR is made up of two arms, the _ and _
The TCR is made up of two arms, the alpha and beta
(True/ False) VDJ recombination occurs in the TCR
True; VDJ recombination occurs in the TCR
* Occurs in the thymus
HLA-A, HLA-B, and HLA-C are all (MHC I/ MHC II)
HLA-A, HLA-B, and HLA-C are all MHC I
HLA- DP, HLA- DQ, HLA-DR are all (MHC I/ MHC II)
HLA- DP, HLA- DQ, HLA-DR are all MHC II
MHC I can be found _
MHC I can be found on all nucleated cells
* RBCs do not have MHC I
MHC II can be found _
MHC II can be found only on professional APCs
Why is it significant that all cells in the body have MHC I?
All cells have MHC I so that we can constantly surveil our cells and kill off malignant/ infected cells if needed (CD8+)
MHC I presents (endogenous/ exogenous) peptides
MHC I presents endogenous peptides
MHC II presents (endogenous/ exogenous) peptides
MHC II presents exogenous peptides
(MHC I/ MHC II) contains two chains (alpha and beta) of equal length
MHC II contains two chains (alpha and beta) of equal length
* Both chains are transmembrane
* Both alpha and beta bind peptide
(MHC I/ MHC II) contains beta2-microglobulin for stability
MHC I contains beta2-microglobulin for stability
In MHC I, only _ chain forms the peptide binding cleft
In MHC I, only alpha chain forms the peptide binding cleft
TAP and proteasome are part of (MHC I/ MHC II) processing and presentation
TAP and proteasome are part of MHC I processing and presentation
The invariant chain is a part of (MHC I/ MHC II) processing and presentation
The invariant chain is a part of MHC II processing and presentation
Steps of MHC I processing and presentation
MHC I:
1. Endogenous, cytosolic protein
2. Antigen is processed in the proteasome which chops it into small peptides
3. Antigen then travels to the transporter associated antigen processing protein (TAP) which gives the antigen access into the ER
4. In the ER, the antigen binds MHC
5. Travels to get expressed on the outside of the cell
Steps of the MHC II processing and presentation
MHC II:
1. Exogenous antigen undergoes endocytosis
2. Invariant chain is involved in MHC biosynthesis
3. MHC and peptide find each other in endocytic vesicle (not in ER)
4. Travels to get expressed on the outside of the cell
CD4+ cells have multiple effector functions:
CD4+:
* Activate macrophages for destruction of phagocytosed antigen
* B cell antibody secretion: antibody binding to antigen
* We need CD4+ to stimulate class switch from IgM to make effective antibodies
T cells originate in the _ but
mature in the _
T cells originate in the bone marrow but
mature in the thymus
VDJ recombination for T cells happens in the _
VDJ recombination for T cells happens in the thymus
Where would we find a CD4+CD8+ cell?
Double positive T cells are still in the maturation process so they could be found in the thymus
MHC II pathway involves loading peptides from the endosome/lysosome (internalized); we rely on _ enzymes to generate peptides
MHC II pathway involves loading peptides from the endosome/lysosome (internalized); we rely on endosomal and lysosomal proteases to generate peptides
* Versus MHC I pathway which uses a proteasome
The peptide loading site onto MHC I is the _
The peptide loading site onto MHC I is the Endoplasmic reticulum
The peptide loading site of MHC II is the _
The peptide loading site of MHC II is the specialized vesicular compartment
Naive T cells will recycle from lymph nodes to the blood seeking encounters from pathogens; if pathogen is not presented, naive T cells die within _
Naive T cells will recycle from lymph nodes to the blood seeking encounters from pathogens; if pathogen is not presented, naive T cells die within 5-7 weeks
The main secondary signal required to activate T cell is _ and _ binding
The main secondary signal is CD28-B7
* A second co-stimulatory signal is required to induce complete T cell activation
* CD28 is on the T cell
* B7 is on the APC
The three most common subtypes of T helper cells are _ , _ , and _
The three most common subtypes of T helper cells are Th1 , Th2 , and Th17
* All of these have different functions and the dendritic cells will tell us what pathogen is out there and decide which T helper cell is needed
Th1 cells secrete _ cytokines
Th1 cells secrete IFN gamma
* Th1 cells are the most commonly used
_ T helper cell is primarily responsible for macrophage activation and IgG production
Th1 is primarily responsible for macrophage activation and IgG production
* Secreted against intracellular microbes
* Associated with autoimmune diseases and tissue damage in chronic infections
_ T helper cell is secreted against helminthic and parasitic infections; it leads to mast cell and eosinophil activation, IgE production
Th2 is secreted against helminthic and parasitic infections; it leads to mast cell and eosinophil activation, IgE production
_ T helper cell is secreted when we have a bacterial or fungal infection; it activates neutrophils and monocytic inflammation
Th17 is secreted when we have a bacterial or fungal infection; it activates neutrophils and monocytic inflammation
Th2 cells secrete _ cytokines
Th2 cells secrete IL-4, IL-5, IL-13
Th17 cells secrete _ cytokines
Th17 cells secrete IL-17, IL-22
CD8+ cells cause apoptosis of target cells by secreting _ and _
CD8+ cells cause apoptosis of target cells by secreting perforin and granzymes
Natural killer cells destroy virally infected cells by binding to surface receptors for _
Natural killer cells destroy virally infected cells by binding to surface receptors for IgG
* IgG is an antibody that coats the antigen for destruction by NK cells
Natural killer cells secrete _ and _
Natural killer cells secrete perforin and granzyme
T lymphocytes undergo central tolerance in the thymus where they have 2 possible routes:
Central tolerance in the thymus:
1. Deleted via negative selection
2. Become Treg cells
B lymphocytes undergo central tolerance in the bone marrow where they have 3 possible routes:
B lymphocytes undergo central tolerance in the bone marrow where they have 3 possible routes:
1. Deletion via negative selection
2. Anergy (bind but inactive)
3. Receptor editing (second chance)
(T lymphocytes/ B lymphocytes) can get a second chance during central tolerance; they undergo receptor editing
B lymphocytes can get a second chance during central tolerance; they undergo receptor editing
Peripheral tolerance happens in _ and _
Peripheral tolerance happens in spleen and lymph nodes
Regulatory T cells will go to _ and inhibit responses against self-antigens by secreting _ and _
Regulatory T cells will go to periphery and inhibit responses against self-antigens by secreting IL-10 and TGF-beta
* They have special transcription factors and markers associated with them (CD3+CD4+CD25 and FoxP3+)
* Their development is independent of AIRE
In addition to inhibitory cytokines, Treg cells also suppress immune response via expression of _ and _
In addition to inhibitory cytokines, Treg cells also suppress immune response via expression of CTLA-4 and IL-2 receptors to capture IL-2
