SMAD2/3 Phosphorylation Is Downregulated in T Cells in HIV-Infected Patients

Persistent inflammation contributes to the exhaustion of immune system and non-AIDS-defining events in HIV-infected patients. Transforming growth factor β (TGF-β) is generally considered an anti-inflammatory cytokine. It is unclear that why high-level TGF-β coexists with chronic inflammation during HIV infection. In this study, it was found that HIV-infected patients had lower proportion of phosphorylated SMAD2/3-positive cells among total CD3⁺ T cells and subsets of CD3⁺CD8⁺ and CD3⁺CD8^- T cells when compared with health subjects. The findings implied that phosphorylation of SMAD2/3 is inhibited in HIV-infected patients, and that disturbance of TGF-β/SMAD2/3 signaling pathway may be involved in HIV-related chronic inflammation.