Polarized helper T cells in tubercular pleural effusion: phenotypic identity and selective recruitment

被引:55
作者
Mitra, DK [1 ]
Sharma, SK
Dinda, AK
Bindra, MS
Madan, B
Ghosh, B
机构
[1] All India Inst Med Sci, Dept Transplant Immunol, New Delhi 110029, India
[2] All India Inst Med Sci, Dept Immunogenet, New Delhi 110029, India
[3] All India Inst Med Sci, Dept Med, Div Pulm & Crit Care Med, New Delhi 110029, India
[4] All India Inst Med Sci, Dept Pathol, New Delhi 110029, India
[5] Inst Genom & Integrat Biol, Mol Immunol & Immunogenet Lab, New Delhi, India
关键词
T cells; chemokines; tuberculosis;
D O I
10.1002/eji.200525977
中图分类号
R392 [医学免疫学]; Q939.91 [免疫学];
学科分类号
100102 ;
摘要
Containment of Mycobacterium tuberculosis critically depends on orchestrated generation of Thl cells and their selective recruitment at the pathologic sites. Understanding the mechanism involved in this process is important for defining better intervention strategies. We investigated the surface phenotype of Thl cells and the role of chemotactic factors in their selective recruitment in tuberculosis pleural effusion and tuberculin site. Memory T cells obtained from the pleural fluid expressed a battery of homing receptors such as CD11a, CCR5 and CXCR3. Similar expression profile was noted on T cells infiltrating the tuberculin site. Expression of their respective ligands such as ICAM-1, RANTES, MIP1-alpha, Mig and IP-10 were detected at pathologic sites. In vitro assay of T cell adherence to activated human umbilical vein endothelial cells (HUVEC) expressing chemotactic ligands suggests an important role of these homing molecules in their selective trafficking. Here, we demonstrate a hierarchy of CXCR3 in effector cell adhesion to HUVEC in vitro, although CD11a and CCR5 were also observed to mediate cell adhesion in an additive fashion. Findings of the present study provide mechanistic insights into the critical events of T cell trafficking in tuberculosis and may help designing better therapeutic modalities.
引用
收藏
页码:2367 / 2375
页数:9
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