LAG3 Expression in Active Mycobacterium tuberculosis Infections

摘要: Mycobacterium tuberculosis (MTB) is a highly successful pathogen because of its ability to persist in human lungs for long periods time. MTB modulates several aspects the host immune response. Lymphocyte-activation gene 3 (LAG3) protein with high affinity CD4 receptor and expressed mainly by regulatory T cells immunomodulatory functions. To understand function LAG3 during infection, nonhuman primate model tuberculosis, which recapitulates key natural infection rhesus macaques (Macaca mulatta), was used. We show that expression induced particularly granulomatous lesions experimentally infected MTB. Furthermore, we not lung granulomas animals exhibiting latent infection. However, simian immunodeficiency virus–induced reactivation results an increased lungs. This response observed primates non-MTB bacterial pathogens, nor virus alone. Our data primarily on CD4+ cells, presumably but also killer cells. The coincides burdens changes type 1 helper T-cell