分泌干扰素γ的细胞和干扰素γ的生物活性

Bioactivity of Interferon gamma(IFNγ )

　

　

　

IFNγ由T辅助细胞（特别是Th1细胞），细胞毒性T细胞（TC细胞），巨噬细胞，粘膜上皮细胞和NK细胞分泌。 IFNγ是唯一的II型干扰素，它在血清学上不同于I型干扰素;它是酸不稳定的，而I型变体是酸稳定的。

 

IFNγ具有抗病毒，免疫调节和抗肿瘤特性。[19]它改变多达30种基因的转录，产生各种生理和细胞反应。其中的影响是：

 

促进NK细胞活动

增加巨噬细胞的抗原呈递和溶酶体活性。

激活诱导型一氧化氮合酶（iNOS）

诱导从活化的血浆B细胞产生IgG2a和IgG3

通过诱导抗原加工基因，包括免疫蛋白酶体的亚基（MECL1，LMP2，LMP7），使正常细胞增加I类MHC分子的表达以及抗原呈递细胞上的II类MHC特异性，以及TAP和ERAAP可能还可能直接上调MHC重链和B2-微球蛋白本身

促进白细胞迁移所需的粘附和结合

诱导内在防御因子的表达 - 例如，对于逆转录病毒，相关基因包括TRIM5alpha，APOBEC和Tetherin，直接代表抗病毒作用

　

IFNγ是定义Th1细胞的主要细胞因子：Th1细胞分泌IFNγ，这反过来导致更多未分化的CD4 +细胞（Th0细胞）分化成Th1细胞[需要引证]，代表正反馈环 - 同时抑制Th2细胞分化。 （其他细胞的等效细胞因子包括Th2细胞的IL-4和Th17细胞的IL-17。）

　

NK细胞和CD8 +细胞毒性T细胞(CTL)也产生IFNγ。 IFNγ通过快速降解RANK-RANKL信号传导途径中的RANK衔接蛋白TRAF6来抑制破骨细胞形成，否则其刺激NF-κB的产生。

　

　

　

Bioactivity of Interferon gamma

 

IFNγ is secreted by T helper cells (specifically, Th1 cells), cytotoxic T cells (TC cells), macrophages, mucosal epithelial cells and NK cells. IFNγ is the only Type II interferon and it is serologically distinct from Type I interferons; it is acid-labile, while the type I variants are acid-stable.

　

IFNγ has antiviral, immunoregulatory, and anti-tumor properties.[19] It alters transcription in up to 30 genes producing a variety of physiological and cellular responses. Among the effects are:

　

Promotes NK cell activity

Increases antigen presentation and lysosome activity of macrophages.

Activates inducible nitric oxide synthase (iNOS)

Induces the production of IgG2a and IgG3 from activated plasma B cells

Causes normal cells to increase expression of class I MHC molecules as well as class II MHC on antigen-presenting cells—to be specific, through induction of antigen processing genes, including subunits of the immunoproteasome (MECL1, LMP2, LMP7), as well as TAP and ERAAP in addition possibly to the direct upregulation of MHC heavy chains and B2-microglobulin itself

Promotes adhesion and binding required for leukocyte migration

Induces the expression of intrinsic defense factors—for example, with respect to retroviruses, relevant genes include TRIM5alpha, APOBEC, and Tetherin, representing directly antiviral effects

IFNγ is the primary cytokine that defines Th1 cells: Th1 cells secrete IFNγ, which in turn causes more undifferentiated CD4+ cells (Th0 cells) to differentiate into Th1 cells[citation needed], representing a positive feedback loop—while suppressing Th2 cell differentiation. (Equivalent defining cytokines for other cells include IL-4 for Th2 cells and IL-17 for Th17 cells.)

NK cells and CD8+ cytotoxic T cells also produce IFNγ. IFNγ suppresses osteoclast formation by rapidly degrading the RANK adaptor protein TRAF6 in the RANK-RANKL signaling pathway, which otherwise stimulates the production of NF-κB.

 

https://en.wikipedia.org/wiki/Interferon_gamma