Th1-specific bystander costimulation imparts resistance against Mycobacterium tuberculosis infection.
The protection against Mycobacterium tuberculosis infection is mediated by T helper type-1 (Th1) cells. Infection of BALB/c mice with M. tuberculosis downregulates expression of a Th1-specific costimulatory molecule, M150, on the surface of infected macrophages. The proliferation of Th cells and Th1-cytokine production by these cells are higher in case of M. tuberculosis antigen presentation by uninfected macrophages than by infected macrophages. The difference in inducing interleukin(IL)-2 and interferon (IFN)-gamma secretion is abolished by providing bystander costimulation through M150 on liposomes.
Das
G
G
National Centre for Cell Science, Ganeshkhind, Pune, India.
Vohra
H
H
Saha
B
B
Mishra
G C
GC
D000818:Animals; D004337:Drug Carriers; D007113:Immunity, Innate; D007371:Interferon-gamma / Q000378:metabolism; D007376:Interleukin-2 / Q000378:metabolism; D015847:Interleukin-4 / Q000378:metabolism; D008081:Liposomes; D008213:Lymphocyte Activation; D017737:Macrophages, Peritoneal / Q000276:immunology*; D008565:Membrane Proteins / Q000276:immunology*; D051379:Mice; D008807:Mice, Inbred BALB C; D009169:Mycobacterium tuberculosis / Q000276:immunology*; D015398:Signal Transduction; D018417:Th1 Cells; D014376:Tuberculosis / Q000276:immunology*
D004337:Drug Carriers; D007376:Interleukin-2; D008081:Liposomes; D008565:Membrane Proteins; D015847:Interleukin-4; D007371:Interferon-gamma