CD8+ T cells recognize and kill cells presenting peptides from viruses or other pathogens through MHC class I molecules. They perform this function through two main mechanisms: 1) secreting cytokines like TNF-α and IFN-γ that have anti-viral and anti-tumor effects, and 2) releasing cytotoxic granules containing perforin and granzymes that form pores in target cells and induce apoptosis. CD4+ T cells help regulate and support the CD8+ T cell response through licensing dendritic cells and promoting interactions between dendritic cells and CD8+ T cells.

1. CD4 & CD8

2. CD8+ (cytotoxic) T cells, like CD4+ Helper T cells, are generated in the thymus and
express the T-cell receptor
CD8+ T cells recognise peptides presented by MHC Class I molecules, found on all
nucleated cells
MHC class I molecules are expressed in all nucleated cells and also in platelets—in
essence all cells but red blood cells. It presents epitopes to killer T cells, also called
cytotoxic T lymphocytes (CTLs)
the CTL triggers the cell to undergo programmed cell death by apoptosis

3. The first is secretion of cytokines, primarily TNF-α and IFN-γ, which have anti-tumour
and anti-viral microbial effects.
The second major function is the production and release of cytotoxic granules. These
granules, also found in NK cells, contain two families of proteins, perforin, and
granzymes. Perforin forms a pore in the membrane of the target cell, similar to the
membrane attack complex of complement
CD8+ T cells are able to release their granules, kill an infected cell, then move to a new
target and kill again, often referred to as serial killing.

4. Following immunization, CD4+ T cells promote the induction of a robust primary
CD8+ T cell response through numerous mechanisms, including licensing of
dendritic cells (DCs) and promoting the interaction between DCs and CD8+ T
cells.
CD4+ T cells regulate the secondary responsiveness of CD8+ T cells during
immunization through suppression of TNF-related apoptosis-inducing ligand
(TRAIL) through a process dependent on licensing of DCs to produce
interleukin-15 (IL-15) and autocrine secretion of IL-2 by CD8+ T cells.

5. Following infection, CD4+ T cell help is necessary for the induction of a memory
CD8+ T cell pool capable of mediating protective immunity but is largely
dispensable for a robust primary response.
During chronic infection, effector CD4+ T cells support the maintenance of
functional CD8+ T cells through secretion of IL-21, whereas TReg cells dampen
the CD8+ T cell response through suppression of DCs.