Mycobacterium Tuberculosis Infection: Participation of TH1, TH2, TH17 and Regulatory T Cells in the Immune Response

Abstract

Mycobacterium tuberculosis, the etiologic agent of Tuberculosis, is a pathogen that is widely distributed geographically. Tuberculosis is classified as a granulomatous inflammatory condition where effector cells accumulate at the site of mycobacterial infection to form the characteristic tubercle. Regulating proteins of Th1 and Th17 cells participate in the formation of Mycobacterium-induced granuloma. The predominance of Th2 phenotype cytokines increases the severity of Tuberculosis. Treg cells are increased in patients with active Tuberculosis but decrease with anti-Tuberculosis treatment. The increment of these cells causes down-regulation of adaptive immune response facilitating the persistence of the bacterial infection. Mycobacterium tuberculosis-induced Treg cells to secrete cytokines that inhibit the immune response. This has been considered an important evasion mechanism although it is not the only that intervenes. The evolution of the Mycobacterium tuberculosis infection will depend on the cytokines' network that traduces pathological change in cells and tissues which explain the clinical manifestations existing in affected patients.

Keywords

• Mycobacterium tuberculosis
• Virulence
• Host genetic
• Immune response
• Cytokines