Regulation of antigen presentation by Mycobacterium tuberculosis: a role for Toll-like receptors

Top Cited Papers
Publisher Website
Google Scholar
Abstract
Mycobacterium tuberculosis survives in the host in antigen-presenting cells (APCs) such as macrophages and dendritic cells. APCs present antigens in association with major histocompatibility complex (MHC) class II molecules to stimulate CD4+ T cells, and this process is essential for containing M. tuberculosis infection. Immune evasion allows M. tuberculosis to establish persistent or latent infection in APCs. M. tuberculosis infection of macrophages results in Toll-like receptor 2 (TLR2)-dependent inhibition of MHC class II transactivator (CIITA) and MHC class II molecule expression and of MHC class II antigen presentation, providing a mechanism for immune evasion. The TLR2-dependent reduction of antigen presentation might reflect a general mechanism of negative-feedback regulation that prevents excessive T cell-mediated inflammation and that M. tuberculosis has subverted for the purposes of immune evasion. Inhibition of antigen presentation creates a niche for M. tuberculosis survival in infected APCs and for its evasion of recognition by CD4+ T cells.

This publication has 150 references indexed in Scilit: