Defective Antigen Presentation Leads to Upregulation of PD1 and IL-10 in HIV-TB Co-Infection

J Interferon Cytokine Res. 2020 Jun;40(6):310-319. doi: 10.1089/jir.2019.0243. Epub 2020 May 22.


Human immunodeficiency virus-tuberculosis (HIV-TB) co-infection poses a challenge to the immunologists in developing new diagnostic and therapeutic tools. Mechanisms behind the breakdown of the immune defense of the co-infected individual are poorly known. Numerous studies in HIV alone have revealed the role of PD1, TAP, and IL-10, but not in co-infection. The interaction of the 2 distinct bugs, which is resulting in domination over the host immune system, is still a lacuna. Hence, we aimed to portray functions of IL-10, TAP, and PD1 molecules in HIV-TB co-infection. Co-culture cells challenged with γ-irradiated M.Tb under various conditions resulted in high interleukin (IL)-10 secretion and high percentage of PD1 expression on CD8 T cells, which might be due to defective antigen presentation of TAP on dendritic cells and macrophages. Herein our observations provide an insight into the escape mechanisms by M.Tb in HIV-infected individuals from the host immune responses leading to TB co-infection.

Keywords: HIV-TB co-infection; IFN-γ; IL-10; PD1; TAP.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Adult
  • Antigen Presentation / immunology
  • Coculture Techniques
  • HIV Infections / immunology*
  • Humans
  • Interleukin-10 / analysis
  • Interleukin-10 / genetics
  • Interleukin-10 / immunology*
  • Mycobacterium tuberculosis / immunology
  • Programmed Cell Death 1 Receptor / analysis
  • Programmed Cell Death 1 Receptor / genetics
  • Programmed Cell Death 1 Receptor / immunology*
  • Tuberculosis / immunology*
  • Up-Regulation*


  • IL10 protein, human
  • PDCD1 protein, human
  • Programmed Cell Death 1 Receptor
  • Interleukin-10