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Cytotoxic T cells (sometimes known as "killer" T cells) are essential adaptive immune system lymphocytes. Similar to helper T cells, antigen-presenting cells in the lymph nodes activate these cells. Cytotoxic T cells directly attack and destroy infected host cells, whereas helper T cells coordinate the action of other immune cells against a pathogen.

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The two major types of T lymphocytes in the human immune system are cytotoxic T cells and helper T cells. Both develop from bone marrow stem cells before moving to the thymus, where they mature and differentiate into CD4+ and CD8+ T lymphocytes, respectively.

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Depending on their function, all T cells express T cell receptors (TCRs) on their surface as well as CD4 or CD8 co-receptors. Helper T cells express CD4 receptors (and are sometimes referred to as CD4+ T cells), whereas cytotoxic T cells express CD8 receptors (and are sometimes referred to as CD8+ T cells).

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Helper T cells manage the adaptive immune response by stimulating other immune cells, whereas cytotoxic T cells kill infected cells directly.

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Before encountering their unique antigen, all T cells are considered "nave." Similarly to helper T cells, cytotoxic T cells recognise only a single type of antigen. However, they cannot bind to their antigen directly; rather, they rely on antigen-presenting cells for assistance (APCs).

Activation of Cytotoxic T Cells

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APCs (such as dendritic cells, macrophages, and B cells) locate and engulf invading pathogens prior to breaking them down into protein pieces. Some of these fragments are exposed to lymph node T lymphocytes on their surface as part of the Major Histocompatibility Complex (MCH).

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When a cytotoxic T cell detects its specific antigen on the surface of an APC, its TCR attaches to the MHC, activating the T cell.

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MCHI and MCHII are the two forms of Major Histocompatibility Complexes present on the surface of APCs. The primary distinction between the activation of helper T cells and cytotoxic T cells is that each kind of T cell binds to a particular MCH receptor. Helper T cells can only bind to MHCII complexes, whereas cytotoxic T cells can bind to MHCI complexes.

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Once an antigen is exposed to a naive T cell, it rapidly multiplies and cytotoxic T cells begin to travel to sites of infection throughout the body.

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Cytotoxic T cells are also referred to as 'killer' T cells due to their ability to destroy infected cells, pathogens, and tumour cells. This is accomplished mostly by the transmission of cytotoxic granules to infected target cells, which kill both the cell and any infections it may contain.

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Cytotoxic T cells and natural killer (NK) cells destroy virus-infected cells and pathogens by an extremely similar method.

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Cytotoxic T cells, like NK cells, have perforin and granzyme-containing cytotoxic granules that kill target cells. Cytotoxic T cells attach to the MHCI via their TCR receptors and release their cytotoxic granules when they encounter infected cells. Granzymes infiltrate target cells through perforin-created pores. Granzymes cause apoptosis, killing the cell and any infections inside.

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Cytotoxic T cells kill virus-infected cells, which aids the host by containing and destroying viruses. The viruses may spread if the cell were lysed.

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NK and cytotoxic T cells distinguish themselves by how they recognise targets. Tumor and pathogen-infected cells lose MHCI, which activates natural killer cells. Cytotoxic T cells detect targets by MCHI complex antigens. Cytotoxic T cells and NK cells are "serial killers" that assault several targets.

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Cytotoxic T cells secrete perforin and granzyme, their major weapon. Cytotoxic T cells release cytokines that aid adaptive immunity.

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IFN-γ directly suppresses viral replication, slowing infection spread. IFN-γ also activates macrophages, which move to infection sites to act as effector cells (engulfing and destroying pathogens) and antigen-presenting cells.

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Cytotoxic T cells are vital to the adaptive immune response and can eliminate contaminated cells. Cytotoxic T cells can cause excessive immune responses that destroy healthy host cells and tissues if left unchecked.

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In most cases, this is prevented by an event known as the contraction phase, which takes place a few weeks after the initial infection. Cytotoxic T cell activity typically peaks around 7 days after the initial infection. In the days and weeks following the peak of cytotoxic T cell activity, the contraction phase begins and up to 95% of the cells die off. The remaining 5-10% become memory T cells, which remain in the body for a long time after the infection has been cleared.