T Cell Pathways Involving CTLA4 Contribute To a Model of Acute Lung Injury

被引：49

作者：

Nakajima, Takeshi ^{[1
]}

Suarez, Carlos Jose ^{[1
]}

Lin, Ko-Wei ^{[1
]}

Jen, Kai Yu ^{[1
]}

Schnitzer, Jan E. ^{[3
]}

Makani, Samir S. ^{[1
]}

Parker, Nathan ^{[1
]}

Perkins, David L. ^{[2
]}

Finn, Patricia W. ^{[1
]}

机构：

[1] Univ Calif San Diego, Dept Med, Div Pulm & Crit Med, La Jolla, CA 92093 USA

[2] Univ Calif San Diego, Dept Med, Div Nephrol, La Jolla, CA 92093 USA

[3] Proteogenom Res Inst Syst Med, San Diego, CA 92121 USA

来源：

JOURNAL OF IMMUNOLOGY | 2010年 / 184卷 / 10期

基金：

美国国家卫生研究院;

关键词：

TOLL-LIKE RECEPTORS; RESPIRATORY-DISTRESS-SYNDROME; NEUTROPHIL RECRUITMENT; LIPOPOLYSACCHARIDE; LYMPHOCYTES; INFLAMMATION; INTERLEUKIN-17; MOUSE; IL-17; MICE;

D O I：

10.4049/jimmunol.0903238

中图分类号：

R392 [医学免疫学]; Q939.91 [免疫学];

学科分类号：

100102 ;

摘要：

Acute lung injury (ALI) is a frequent pulmonary complication in critically ill patients. We characterized a murine model of LPS-induced ALI, focusing on Th cells. Following LPS administration, bronchoalveolar lavage lymphocytes, neutrophils, IL-6, TNF-alpha, and albumin were increased. Analysis of LPS-induced T cells revealed increased Th cell-associated cytokines (IL-17A, -17F, and -22), as well as increased expression of CD69 (a cell activation marker), Foxp3, and CTLA4 in CD4(+) T cells. Administration of anti-CTLA4 Ab decreased LPS-induced bronchoalveolar lavage 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. The Journal of Immunology, 2010, 184: 5835-5841.

引用

页码：5835 / 5841

页数：7

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