Toll-like receptor 2 in host defense against Mycobacterium tuberculosis: to be or not to be — that is the question. (October 2016)

• Record Type: Journal Article
• Authors: Gopalakrishnan, Archana; Salgame, Padmini
• Is Part Of: Current opinion in immunology. Volume 42(2016)
• Page Start: 76
• Page End: 82
• Publication Date: 2016-10
• Subjects: Immunology -- Periodicals; Allergy -- Periodicals; Immunology -- Abstracts -- Periodicals; Allergy -- Abstracts -- Periodicals; 616.079
• DOI: 10.1016/j.coi.2016.06.003
• Languages: English
• ISSNs: 0952-7915

Abstract

Highlights: TLR2 does not contribute to protection against acute Mtb infection. TLR2 has a significant role in protection against chronic Mtb infection. TLR2 controls immunopathology in chronic Mtb infection. Mtb hijacks TLR2 to evade macrophage effector mechanisms. TLR2 signaling is regulated to minimize host immunopathology. Abstract : Toll-like receptor (TLR) 2 is expressed on immune cells and respiratory epithelial cells lining the lung. TLR2 is not critical for protection during acute Mycobacterium tuberculosis (Mtb) infection but it has a significant multi-faceted role in containing chronic infection. This review highlights the contribution of TLR2 to host protection, immune evasion by Mtb and immune regulation during chronic Mtb infection. The TLR2-triggered pro-inflammatory cytokines initiate protective mechanisms and limit Mtb replication while the immune evasion pathways counterattack anti-bacterial effector mechanisms. The immune regulation pathways that are activated dampen TLR2 signaling. The combinatorial effect of these functional responses is persistence of Mtb with minimal immunopathology.