All viruses, and some bacteria, multiply in the cytoplasm of infected cells. Once inside cells, these pathogens are not accessible to attack by antibodies and can be eliminated only by the destruction of the infected cells. These infected cells are destroyed by Cytotoxic T Cells, a subset of T lymphocytes that express the CD8 glycoprotein (CD8+) on their surface.
Cytotoxic T Cells form part of the adaptive immune system and fulfill a role similar to that of the NK cell in the innate immune system. These cells survey the body for the presence of virus-infected and cancerous cells, which they kill by inducing the target cell to apoptose. The elimination of infected cells without the destruction of healthy tissue requires the cytotoxic mechanisms of CD8 T cells to be both powerful and accurately targeted.
Viral and mutant proteins are found inside infected or cancerous cells. Cells degrade their endogenous proteins via antigen processing, resulting in peptide fragments, some of which are presented by MHC Class I to the T cell antigen receptor (TCR) on CD8+ T cells. Virally infected or cancerous cells will present some viral or mutant protein peptide fragments via MHC class I in this manner. If the T Cell Receptor (TCR) on the cytotoxic T cell is specific for that antigen, it binds to the complex of the class I MHC molecule and the antigen, and the CD8+ T cell destroys the infected cell.
Cytotoxic T cells release the cytotoxins perforin, granzymes, and granulysin in order to kill their target cells. Perforin forms pores in the cell membrane of the target cell, creating an aqueous channel through which granzyme and granulysin can enter. Once in the cytoplasm the target cell the serine protease function of granzyme triggers the caspase cascade, which is a series of cysteine proteases that eventually lead to apoptosis.
CD8+ T cells also release the cytokines Interferon-γ (IFN- γ), TNF-α, and TNF-β, which contribute to the immune response. IFN-γ directly inhibits viral replication, and induces the increased expression of MHC class I in infected cells. This increases the chance that infected cells will be recognised as target cells by CD8+ T cells. IFN-γ also activates macrophages, recruiting them to sites of infection both as effector cells and as antigen-presenting cells.
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Resources for in vitro Differentiation and Expansion:
T Cells |
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Molecule |
Species |
Source |
Catalog # |
IL-2 |
Human |
E. coli |
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Mouse |
E. coli |
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Rat |
E. coli |
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Antibodies |
Species |
Clone |
Catalog # (Applications) |
CD3 |
Human |
UCHT1 |
MAB100 (FA, FC, ICC/IF, IP) |
Mouse |
145-2C11 |
MAB484 (Depl., FA, FC, IP) |
|
CD28 |
Human |
37407 |
MAB342 (FA, WB) |
Human |
Polyclonal |
AF-342-PB (FA, FC, ICC/IF, IHC) |
|
Mouse |
794716 |
MAB4832 (FA, FC) |
Cytokine-induced Killer (CIK) Cells |
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Molecule |
Species |
Source |
Catalog # |
IL-2 |
Human |
E. coli |
|
Mouse |
E. coli |
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Rat |
E. coli |
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IFN-g |
Human |
E. coli |
|
Human |
HEK293 |
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Mouse |
E. coli |
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Rat |
E. coli |
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Antibodies |
Species |
Clone |
Catalog # (Applications) |
CD3 |
Human |
UCHT1 |
MAB100 (FA, FC, ICC/IF, IP) |
Mouse |
145-2C11 |
MAB484 (Depl., FA, FC, IP) |
Click on the images below to find out more about other immune cell types.