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… Click to show full abstract
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 the present study, it was found that HIV-infected patients had lower proportion of phosphorylated Smad2/3-posive 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/Smad signaling pathway may be involved in HIV-related chronic inflammation.
               
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