Dendritic cells deal with first encounters of a pathogen. Macrophages support the immune response with continued antigen presentation to T cells. B cells have a late but effective response; they are also prepared in case of a second encounter.
Helper/Killer T cell activation by APC
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| Antigen presentation by Sjef |
- The T cell comes in contact with an APC by weak adhesion molecules as TCR binds MHC.
- T cell upregulates CD40L, which binds CD40 on APC.
- This stimulates MHC and B7, or other costimulating molecules, on the APC. (B7 ligates CD28).
- Costimulation amplifies the TCR signal. This is important for naive T cell activation, whereas costimulation is not needed in activated T cells.
- More efficient T cell activation.
(Not shown in image). CD4 or CD8 also act like a "clip" to strengthen the adhesion of the TCR and MHC. With cytotoxic T cells, CD8 binds MHC I. With helper T cells, CD4 binds MHC II.
αβ T cell signaling
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| TCR Complex by Anriar |
TCR made of α and β chains, for antigen recognition. The TCR comes into contact with antigen-loaded MHC molecules.
CD3 made of four peptide chains: γ, δ and ε associate with the TCR; the ζ-chain generates an intracellular activation signal.
Th cytokines
Helper T cells respond specifically to a pathogen by producing cytokines.
Th1 (classical subset against viruses and bacteria)
- IL-2, the growth factor of CTL and NK cells. Therefore, when many CTLs are needed in a viral infection, the Th cell controls the strength of the cytotoxic T cell response.
- IFN-γ, which primes macrophages and influences IgG class switch in B cells.
- TNF, which activates macrophages and NK cells.
Th2 (parasitic or mucosal subset)
- IL-5, which encourages B cell IgA production.
- IL-10, which downregulates Th1 cytokines and enhances B cell survival and proliferation.
- IL-4, a B cell growth factor; influences IgE class switch in B cells.
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