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Cell-mediated immunity
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==Type 1 immunity== Type 1 immunity makes use of the type 1 subset for each of these cell types. By secreting [[interferon gamma]] and [[TNF]], T<sub>H</sub>1, T<sub>C</sub>1, and group 1 ILCS activate macrophages, converting them to potent effector cells. It provides defense against intracellular [[bacteria]], [[protozoa]], and [[viruses]]. It is also responsible for [[inflammation]] and [[autoimmunity]] with diseases such as [[rheumatoid arthritis]], [[multiple sclerosis]], and [[inflammatory bowel disease]] all being implicated in type 1 immunity. Type 1 immunity consists of these cells:<ref name="The 3 major types of innate and adaptive cell-mediated effector immunity." /> * CD4+ T<sub>H</sub>1 cells * CD8<sup>+</sup> cytotoxic T cells (T<sub>c</sub>1) * T-Bet<sup>+</sup> [[interferon gamma]] producing group 1 ILCs(ILC1 and Natural killer cells) '''CD4<sup>+</sup> T<sub>H</sub>1 Cells''' It has been found in both [[mice]] and [[humans]] that the signature cytokines for these cells are [[interferon gamma]] and [[lymphotoxin alpha]]. The main cytokine for differentiation into T<sub>H</sub>1 cells is IL-12 which is produced by [[dendritic cell]]s in response to the activation of [[pattern recognition receptor]]s. [[T-bet]] is a distinctive [[transcription factor]] of T<sub>H</sub>1 cells. T<sub>H</sub>1 cells are also characterized by the expression of chemokine receptors which allow their movement to sites of inflammation. The main [[chemokine receptors]] on these cells are [[CXCR3A]] and [[CCR5]]. [[Epithelial cells]] and [[keratinocytes]] are able to recruit T<sub>H</sub>1 cells to sites of infection by releasing the chemokines [[CXCL9]], [[CXCL10]] and [[CXCL11]] in response to [[interferon gamma]]. Additionally, [[interferon gamma]] secreted by these cells seems to be important in downregulating [[tight junctions]] in the epithelial barrier.<ref name="The 3 major types of innate and adaptive cell-mediated effector immunity." /> '''CD8<sup>+</sup> T<sub>C</sub>1 Cells''' These cells generally produce [[interferon gamma]]. Interferon gamma and [[Interleukin 12|IL-12]] promote differentiation toward T<sub>C</sub>1 cells. [[T-bet]] activation is required for both interferon gamma and cytolytic potential. [[CCR5]] and [[CXCR3]] are the main chemokine receptors for this cell.<ref name="The 3 major types of innate and adaptive cell-mediated effector immunity." /> '''Group 1 ILCs''' Groups 1 ILCs are defined to include [[Innate lymphoid cell|ILCs]] expressing the transcription factor [[T-bet]] and were originally thought to only include [[natural killer cell]]s. Recently, there have been a large amount of NKp46<sup>+</sup> cells that express certain master [transcription factor]s that allow them to be designated as a distinct lineage of natural killer cells termed ILC1s. ILC1s are characterized by the ability to produce [[interferon gamma]], [[TNF]], [[GM-CSF]] and [[Interleukin 2|IL-2]] in response to cytokine stimulation but have low or no cytotoxic ability.<ref name="The 3 major types of innate and adaptive cell-mediated effector immunity." />
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