T cell pathways involving CTLA4 contribute to a model of acute lung injury.
T cell pathways involving CTLA4 contribute to a model of acute lung injury.
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涉及CTLA4的T细胞途径有助于急性肺损伤模型。
DOI：
10.4049/jimmunol.0903238
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发表时间：
2010-05-15
期刊：
影响因子：
--
通讯作者：
Finn PW
中科院分区：
文献类型：
--
作者：
Nakajima T;Suarez CJ;Lin KW;Jen KY;Schnitzer JE;Makani SS;Parker N;Perkins DL;Finn PW
Acute lung injury (ALI) is a frequent pulmonary complication in critically ill patients. We characterized a murine model of LPS-induced ALI, focusing on T helper cells. Following LPS administration, BAL lymphocytes were increased as well as neutrophils, IL-6, TNF-α, and albumin. Analysis of LPS-induced T cells revealed increased T helper cell associated cytokines (IL-17A, IL-17F, and IL-22), expression of CD69, a cell activation marker, forkhead box P3 (Foxp3), and cytotoxic T lymphocyte antigen 4 (CTLA4) in CD4+ T cells. Administration of anti-CTLA4 antibody decreased LPS-induced BAL albumin and IL-17A, while increasing CD4+Foxp3+ cell number and Foxp3 expression in CD4+Foxp3+ cells. These data suggest that pulmonary LPS administration promotes CD4+ T cells and that T cell pathways involving CTLA4 contribute to ALI.
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