Effects of Helicobacter pylori infection on T cell activation markers and regulatory T cells in people with and without HIV infection in Central Ethiopia.

backgroundHelicobacter pylori (H. pylori) is known to modulate host immunity and sustain chronic inflammation, yet most data come from HIV-negative populations. In people living with HIV, whose T cell compartments are already dysregulated, the way H. pylori shapes peripheral T cell phenotypes, and how those profiles change after eradication therapy, is still unclear. Because both infections are common in Central Ethiopia, we examined peripheral T cell phenotypes in adults with and without HIV according to H. pylori status and assessed the immunologic effects of antibiotic eradication. MATERIALS AND

methodsWe conducted a prospective study in people with and without HIV infection from Ethiopia. H. pylori status was determined by stool-antigen testing; a subset received standard triple therapy and was followed for 12 months. Multiparameter flow cytometry quantified T cell activation, proliferation, exhaustion, and regulatory T cells (T

resultsT cell analyses showed that participants with HIV had consistently higher proliferation (Ki67), exhaustion (PD-1, TIM3), and Th17 (CCR6⁺CD161⁺) markers than those without HIV. H. pylori-positive individuals exhibited higher T

conclusionsH. pylori infection was linked to significant differences in T cell profiles in both HIV-negative and HIV-positive individuals. Eradication therapy was followed by a reduction in Tregs-significant in HIV-negative participants irrespective of outcome and in PLWH with successful eradication-with subgroup-specific shifts in activation and differentiation/exhaustion markers, highlighting potential therapeutic avenues for mitigating immune dysregulation in co-infected populations.