CCR4-dependent reduction in the number and suppressor function of CD4+Foxp3+ cells augments IFN-γ-mediated pulmonary inflammation and aggravates tuberculosis pathogenesis.

摘要: Chronic pulmonary inflammation marked predominantly by CD4+IFN-γ+ cells is the hallmark of tuberculosis pathogenesis in immunocompetent adults, who are substantially affected this disease. Moreover, CD4+Foxp3+ cell-mediated suppression contributes to infection susceptibility. We addressed role pathogenesis, because aspect has not been during chronic infection. targeted CCR4, which induces influx into lungs. CCR4−/− mice exhibited a lower frequency at 15, 30, and 70 days than their wild-type counterparts. However, only was an exacerbated IFN-γ-mediated immune response associated with apparent In addition, decrease suppressor function cells. Adoptive transfer Foxp3+ infected restored bacterial load levels observed mice. Our findings suggest that play time-dependent highlight CCR4 plays critical balance regulating translationally relevant, as or could be target for immunotherapy, considering heterogeneity adults.