Effector T-Lymphocytes Flashcards
When can TCR’s recognise foreign peptides?
Once they’ve been processed and put into the context of MHC
Summarise CD8 T cell function
DC recognises the antigen - moves to the lymph node - meets the T cell - T cell migrates to the source of infection
What happens to some of the effector cell once the infection has been cleared?
They become memory cells
What three signals need to be present to license a CD8 response?
Antigen recognition, costimulation (surface surface reaction between the dendritic and T cells) and cytokine release
When do viral peptides get presented in MHC class I?
When a protein is made incorrectly accidentally, so is packaged off and presented
Summarise how T cells lyse cells
The MHC and TCR bind, and through actin repolarization the CD8/CTL cell moves the toxic granules to the site of infection. Apoptosis occurs
Which two methods are available for induced apoptosis?
Perforin and granzyme, and the fas-fas ligand
Explain the perforin + granzyme method for inducing apoptosis
CD8 cell injects perforin into the membrane of the target cell. This makes a pore in the membrane and allows granzyme to enter the cell. Granzyme is an enzyme that stimulates apoptosis by binding to caspases.
Explain the fas-fas ligand mechanism
The fas ligand on the CD8 cell binds to the fas receptor on the target cell, and when engaged it releases caspases
What does caspase do?
Drives apoptosis
How many cells can a CD8 cell target?
Many
4 effector functions of T helper cells?
Macrophage activation, delayed type hypersensitivity response, B cell activation and regulation
Explain T helper cell function regarding macrophages. What T helper cell activates macrophages? What does the macrophage do once activated? How do macrophages and TH cells communicate?
TH1. They release pro inflammatory molecules such as TNF and CD40. They communicate with cytokines.
Explain the function of delayed type hypersensitivity. What can it do if antigens aren’t eradicated or if the antigen is not a microbe?
Main role is defence against intracellular pathogens. Isn’t eradicated: chronic stimulation and granuloma formation. Not a microbe: tissue injury with no protection, “hypersensitivity”.
What are the two phases of delayed type hyper sensitivity?
Sensitisation - exposure to the antigen. Effector - second exposure triggers a severe response.
Two types of delayed type hyper sensitivity?
Th1 specific - macrophage activation for killing intracellular pathogens. Th2 specific - eosinophil activation for killing multicellular pathogens.
What causes immediate hypersensitivity?
Mast cell degranulation
What are the five families of T helper cells?
Th 1 (pro inflammatory and activates macrophages), th 2 boosts multicellular organism responses and activates B cells, follicular helper T cells generates isotope switched antibodies, Th17 important for control and bacteria and arthritis, and Treg that regulate the effector function of other T cells.
Why is Treg crucial?
Necessary to maintain tolerance for self antigens
Difference between B and T memory cells?
T cells don’t undergo affinity maturation
What are the two types of memory T cells? Which lasts longer?
Effector memory (local to site of infection) and central memory (in spleen and lymph nodes, lasts longer)
CCR7-CD45RA- gives what memory cells?
Effector
CCR7+CD45RA- gives what memory cells?
Central
Problem with T cell reactions over time?
T cell level contracts over time, in chronic infections this is a problem
Pathological reactions caused by T cells? (2)
Autoimmunity and rejection of transplants
