Regulation of antigen presentation by Mycobacterium tuberculosis: a role for Toll-like receptors.
Mycobacterium tuberculosis survives 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 to contain M. tuberculosis infection. Immune evasion allows M. tuberculosis to establish persistent or latent infection in macrophages and results in Toll-like receptor 2 (TLR2)-dependent inhibition of MHC class II transactivator expression, MHC class II molecule expression and antigen presentation. This 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 to create a niche for survival in infected macrophages and evasion of recognition by CD4(+) T cells.
Department of Pathology, Case Western Reserve University, Cleveland, Ohio 44106-7288, USA. cvh3@cwru.edu
Clifford V
CV
Harding
W Henry
WH
Boom
D017951:Antigen Presentation; D000938:Antigen-Presenting Cells / Q000276:immunology; D000942:Antigens, Bacterial / Q000302:isolation & purification; D005802:Genes, MHC Class II; D007371:Interferon-gamma / Q000378:metabolism; D009169:Mycobacterium tuberculosis / Q000235:genetics / Q000276:immunology* / Q000378:metabolism; D013601:T-Lymphocytes / Q000276:immunology / Q000378:metabolism; D051193:Toll-Like Receptors / Q000378:metabolism*
D000942:Antigens, Bacterial; D051193:Toll-Like Receptors; D007371:Interferon-gamma