# Immune Dysregulation in HIV-TB Co-Infection: Role of Cytokines and T Cell Biomarkers—A Narrative Review

## TL;DR

This review explores how immune dysregulation in HIV-TB co-infection affects cytokine and T cell biomarkers, highlighting the need for more research into their roles in disease progression.

## Contribution

The paper synthesizes current evidence on cytokine and T cell biomarker profiles in HIV-TB co-infection, emphasizing gaps in understanding their mechanistic roles.

## Key findings

- Cytokines like IL-17A, IFN-γ, TNF, and T cell markers CD38 and HLA-DR are elevated in active TB compared to latent TB in HIV-infected individuals.
- Immune activation is heightened in HIV-TB co-infection, involving both innate and adaptive immune responses.
- Observational data dominate current findings, with limited mechanistic understanding of immune dysregulation in HIV-TB co-infection.

## Abstract

Immune dysregulation is a hallmark of human immunodeficiency virus (HIV) infection, characterized by persistent immune activation and systemic inflammation that drive T cell exhaustion and senescence, contributing to disease progression and non-AIDS comorbidities, most notably tuberculosis (TB). With rising HIV prevalence, the incidence of HIV-TB co-infection continues to rise, highlighting the need to understand their immunopathological interplay. This narrative review aims to examine the association between immune dysregulation in HIV-TB co-infection, with a focus on cytokine profiles and immunological biomarkers. Relevant literature was retrieved from multiple databases, with evidence demonstrating differential expression of cytokines—IL-17A, IFN-γ, TNF, IL-10, IL-6, IL-4, and IL-2—and T cell activation markers, such as CD38 and HLA-DR on CD4+ T cells in latent and active TB among HIV-infected individuals. These immune mediators are consistently co-expressed at higher levels in active TB compared to latent TB, suggesting heightened immune activation of both innate and adaptive immune responses in HIV-TB co-infection. However, these findings are largely based on observational data, and the precise mechanism by which cytokine and T cell biomarker dysregulation contributes to HIV-TB pathogenesis remains incompletely understood, underscoring the need for larger, mechanistic studies to address these gaps in the pathogenic pathway.