Functional evaluation of immunoregulatory molecules HLA-G, galectin-1, and IL-10 in people living with HIV

• Type of Material: Article
• Authors: Natalia A Cortelette, Federal University of Espírito Santo; Nayana De Oliveira Souza, Federal University of Espírito Santo; Lilian Cataldi-Rodrigues, Fac Pharmaceut Sci Ribeirao Preto USP; Connie Arthur, Emory University; Sean Stowell, Emory University; Marcelo Dias-Baruffi, Fac Pharmaceut Sci Ribeirao Preto USP; Daniela Amorim Melgaco Guimaraes, Federal University of Espírito Santo; Lorena R Ayres, Federal University of Espírito Santo; João Alexandre Trés Pancoto, Federal University of Espírito Santo
• Language: English
• Date: 2022-01-14
• Publisher: LIPPINCOTT WILLIAMS & WILKINS
• Publication Version: Final Published Version
• Copyright Statement: © 2022 the Author(s). Published by Wolters Kluwer Health, Inc.
• License: Creative Commons Attribution-NonCommercial 4.0 International
• Final Published Version (URL): http://dx.doi.org/10.1097/MD.0000000000028489
• Title of Journal or Parent Work: MEDICINE
• Volume: 101
• Issue: 2
• Start Page: E28489
• End Page: E28489
• Grant/Funding Information: This work was supported by Federal University of Espírito Santo, FAPES Research Agency (#139/2019).
• Keywords: CELL-ACTIVATION; Medicine, General & Internal; TO-CHILD TRANSMISSION; galectin-1; CYTOKINE PRODUCTION; interleukin-10; polymorphisms; human leukocyte antigen-G; POLYMORPHISMS; REGULATED EXPRESSION; comorbidities; ASSOCIATION; INTERLEUKIN-10; Life Sciences & Biomedicine; PROGRESSION; 3' UNTRANSLATED REGION; Science & Technology; General & Internal Medicine; GENETIC-VARIANTS; HIV
• Research Categories: Health Sciences, Pathology

Abstract

Objective(s): Investigate polymorphisms and expressions of human leukocyte antigen-G (HLA-G), galectin-1 (Gal-1), and interleukin-10 (IL-10) in people living with HIV (PLHIV) with and without comorbidities to help understanding the mechanisms involved in triggering these disorders in PLHIV and in their prognosis. Design: Here we evaluated the potential correlation between the genetic polymorphism and/or protein levels of HLA-G, Gal-1, and IL-10 with and without comorbidities of PLHIV. Methods: Two hundred HIV patients under antiretroviral treatment (83 with comorbidities and 117 without comorbidities) and 200 healthy individuals (controls) were genotyped, using PCR, for HLA-G 14-base pair polymorphism located at the 3' untranslated region in exon 8insertion/insertion (Ins/Ins: Low HLA-G expression) or deletion/deletion (Del/Del: High HLA-G expression). Soluble levels of HLA-G (sHLA-G), Gal-1, and IL-10 were quantified by enzyme-linked immunosorbet assay. Results: HIV patients without comorbidities exhibited higher frequency of 14-base pair Del/Del genotype than HIV patients with comorbidities. As expected, HIV patients Ins/Ins with and without comorbidities produced less sHLA-G than controls. However, HIV patients Del/Del with comorbidities expressed sHLA-G more than controls and HIV patients Del/Del without comorbidities. Interestingly, patients that showed low levels sHLA-G, and presence of comorbidities, exhibited high Gal-1 serum levels. However, an increase in soluble levels of IL-10 in PLHIV was observed when compared to controls, especially in the PLHIV group without comorbidities suggesting, a protective role of IL-10 in the development of comorbidities. Conclusions: These data suggested that the high expression of sHLA-G and IL-10 or Gal-1 could be associated and could be associated with the development or not of comorbidities in PLHIV.