Myeloid-specific HNRNPA2B1 deficiency disrupts macrophage function and in vivo responses.

ABSTRACT: The mechanisms through which heterogeneous nuclear ribonucleoprotein A2B1 (HNRNPA2B1) contributes to innate immune gene regulation are poorly understood. To fill this gap, we generated a myeloid lineage-specific HNRNPA2B1-conditional mouse using LysMCre. In an endotoxic shock model, HNRNPA2B1-deficient mice exhibit dampened expression of inflammatory mediators despite increased infiltration of macrophages and neutrophils. Likewise, during infection with the gram-negative bacterial pathogen Salmonella enterica, HNRNPA2B1-deficient mice fail to mount protective inflammatory responses and experience higher bacterial burdens. To better understand the molecular mechanisms driving these phenotypes in vivo, we performed transcriptomics analysis of LPS-treated HNRNPA2B1-deficient macrophages ex vi

SUBMITTER: Salih MM 

PROVIDER: S-EPMC12394992 | biostudies-literature | 2025 Aug

REPOSITORIES: biostudies-literature