Expression of killer inhibitory receptors on cytotoxic cells from HIV-1-infected individuals

Abstract

Dysfunction of cytotoxic activity of T and natural killer (NK) lymphocytes is a main immunological feature in patients with AIDS, but its basis are not well understood. It has been recently described that T and NK cell-mediated cytotoxicity can be regulated by HLA killer inhibitory receptors (KIR). In this work, we have determined on cytotoxic T cells and NK cells from HIV-1-infected individuals the expression of the following KIR molecules: p58, p70, and ILT2 (immunoglobulin-like family KIR) as well as CD94 and NKG2A (C-lectin-type family KIR). With some exceptions, no significant changes were found on the expression of immunoglobulin-like KIR in either CD8+ or CD56+ cells. Interestingly, the percentages of CD8+ and CD56+ cells expressing CD94 were significantly increased in these individuals. We also show that, in vitro, IL-10 up-regulates CD94 expression on CD8+ and CD56+ cells obtained from normal individuals, suggesting that the augmented expression observed in HIV-infected individuals could be related to the high levels of IL-10 previously described in HIV-1-infected individuals.

The gp49B1 Inhibitory Receptor Regulates the IFN-γ Responses of T Cells and NK Cells

“…A number of studies have shown that KIRs are expressed by memory/effector CTL under conditions of chronic Ag stimulation, such as tumors and HIV infection, leading to the view that the NK-IRs perhaps serve to reduce CTL-mediated immunopathology after protracted antigenic stimulation (3)(4)(5)(6)(7)(8)(9)(10)(11)(12). Although these studies authenticate that CTL can express NK-IRs under certain situations, their role in a primary immune response in vivo was not clear.…”

Differential Potency and Breadth of the Same Epitope-Specific CTLs to Inhibit HIV-1 Replication based on TCR Usage

“…In addition, numerous regulatory proteins have been reported to induce on T cells during chronic HIV-1 and biologically affect T cell function [36][37][38]. Here, no difference of expression of a panel of T-cell exhaustion and activation-related genes (PD-1, CTLA-4, KLRG1, GRAIL, Itch and Cbl-b) was observed for these TCR-clonotypic clones, indicating that these regulatory proteins did not account for the differential antiviral efficacy of these clones.…”

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

“…Study of Tarazona et al (2002) [45] observed an increase of CD56-CD94+ cells in HIV+ patients, corroborating studies that reinforce the increasing of the CD56neg population in these patients. Study of Galiani et al (1999) [46] observed an increase of NK and T cells expressing CD94. The same author describes a possible association between IL-10 and CD94 expression in these cells.…”