Figure 2.

Responses of the STAT3 signal pathway and Th17-like T cells that are dysregulated or impaired in patients with TB. In TB patients, T-cell exhaustion coincides with a high expression of PD-1 and downregulation of the IL-23 receptor. Thus, stimulation with IL-23 and Mtb antigens cannot induce adequate expression of STAT3. The phosphorylation of STAT3 is also decreased. Mechanistically, two miRNAs targeting STAT3 are highly expressed, and they could inhibit the expression and phosphorylation of STAT3. Consequently, the production of IL-17 is reduced. IL, interleukin; miRNA, microRNA; Mtb, Mycobacterium tuberculosis; PD-1, programmed death-1; RORγt, retinoic acid receptor-related orphan receptor-γt; STAT3, signal transducer and activator of transcription 3; TB, tuberculosis; Th17, T helper 17.