A cross-sectional study of C-type lectin receptors (CD94 and CD314) in patients with HIV/AIDS and cancer

The HIV-1 induces functional and phenotypic changes in the activation profile of NK cells. The cancers arising from immunosuppression induce an increase of pro-inflammatory cytokines in the tumor microenvironment, which can result in altered expression of these receptors in lymphocyte subpopulations, including T lymphocytes, NK cells and NKT cells. In the current study, we investigated possible HIV/AIDS-related changes in the expression of the C-type lectin receptors comparing healthy donors, HIV/AIDS patients, and HIV/AIDS patients with cancer (HIV/AIDSWC). The expression of these receptors was examined in the total NK cell population and CD56dim and CD56bright NK cell subsets separately and T- and NKT-cell populations. There was a significant increase of the expression of NKG2D (CD134) in T lymphocytes in HIV/AIDS and HIV/AIDSWC compared to healthy donors. There were no significant changes of this receptor in NK cells (and their subtypes) and NKT to compare them with healthy donors. As for the CD94 receptor, there were no significant changes of this receptor on NK cells (and their subtypes), NKT cells and T Lymphocyte to compare them with healthy donors, except for the increase in percentage of the expression in CD56bright cells, however this was not true in absolute terms.