期刊
IMMUNITY
卷 21, 期 4, 页码 589-601出版社
CELL PRESS
DOI: 10.1016/j.immuni.2004.09.002
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资金
- NIAID NIH HHS [AI 37618] Funding Source: Medline
- NICHD NIH HHS [5T32 HD 43010] Funding Source: Medline
- NIDDK NIH HHS [DK 49786] Funding Source: Medline
Cytotoxic T lymphocytes and natural killer cells use the perforin/granzyme pathway to kill virally infected cells and tumor cells. Mutations in genes important for this pathway are associated with several human diseases. CD4(+) T regulatory (Treg) cells have emerged as important in the control of immunopathological processes. We have previously shown that human adaptive Treg cells preferentially express granzyme B and can kill allogeneic target cells in a perforin-dependent manner. Here, we demonstrate that activated human CD4(+)CD25(+) natural Treg cells express granzyme A but very little granzyme B. Furthermore, both Treg sub-types display perforin-dependent cytotoxicity against autologous target cells, including activated CD4(+) and CD8(+) T cells, CD14(+) monocytes, and both immature and mature dendritic cells. This cytotoxicity is dependent on CD18 adhesive interactions but is independent of Fas/FasL. Our findings suggest that the perforin/granzyme pathway is one of the mechanisms that Treg cells can use to control immune responses.
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