TIM-3 ameliorates host responses to Salmonella infection by controlling iron driven CD4⁺ T cell differentiation and interleukin-10 formation.

ABSTRACT:

Background

Iron loading increases infection risk in being a nutrient for invading siderophilic bacteria and by modulating immune functions including the expression of the immune checkpoint regulator T-cell immunoglobulin-and-mucin-containing-domain-3 (TIM-3). TIM-3 affects specific immune cell functions including T-helper cell differentiation but also T cell dysfunction, and immune exhaustion. Given the prevalence of iron overload specifically in patients at higher risk for infection such as those suffering from hemo-oncological diseases, we investigated TIM-3's role in immune control of bacterial sepsis.

Methods

A sepsis model was employed in wildtype and Tim3^-/- mice with transgenic expression of a functional natural resistance associated macrophage protein 1 (N

SUBMITTER: Pfeifhofer-Obermair C 

PROVIDER: S-EPMC12571576 | biostudies-literature | 2025 Oct

REPOSITORIES: biostudies-literature