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

Authors

  • Dipendra K. Mitra,

    Corresponding author
    1. Departments of Transplant Immunology and Immunogenetics, All India Institute of Medical Sciences, Ansari Nagar, New Delhi, India
    • Transplant Immunology & Immunogenetics, All India Institute of Medical Sciences, Ansari Nagar, New Delhi 110029, India, Fax: 91-11-265 88663
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  • Surendra K. Sharma,

    Corresponding author
    1. Division of pulmonary and Critical Care medicine, Department of Medicine, All India Institute of Medical Sciences, Ansari Nagar, New Delhi, India
    • Division of pulmonary and Critical Care medicine, Department of Medicine, All India Institute of Medical Sciences, Ansari Nagar, New Delhi 110029, India
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  • Amit K. Dinda,

    1. Department of Pathology, All India Institute of Medical Sciences, Ansari Nagar, New Delhi, India
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  • Manjit S. Bindra,

    1. Departments of Transplant Immunology and Immunogenetics, All India Institute of Medical Sciences, Ansari Nagar, New Delhi, India
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  • Babita Madan,

    1. Molecular Immunology and Immunogenetics Laboratory, Institute of Genomics and Integrative Biology, New Delhi, India
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  • Balaram Ghosh

    1. Molecular Immunology and Immunogenetics Laboratory, Institute of Genomics and Integrative Biology, New Delhi, India
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Abstract

Containment of Mycobacterium tuberculosis critically depends on orchestrated generation of Th1 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 Th1 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-α, 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.

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