Mays Mohammed Salih

UC Santa Cruz

“HNRNPA2B1 promotes interferon response signaling in macrophages and impacts mouse response and survivaal outcome in infection models”

I study regulation of the innate immune response which is our first line of defense against pathogens. I found HNRNPA2B1 which is an RNA processing protein to regulate the inflammatory gene activation post stimulus and to impact mouse survival outcome in infection models.


The innate immune system is the first line of defense against pathogens; it functions through various pattern recognition receptors (PRRs) that recognize microbial products or danger signals leading to the activation of signaling pathways which initiate transcription of inflammatory genes. Activation of the innate immune response is essential to resolve infections, however, its dysregulation can result in pathological inflammation, contributing to an array of diseases, such as atherosclerosis, autoimmunity and cancer. Our understanding of the mechanisms and genes that regulate this response is not yet complete. We have recently found HNRNPA2B1, a ubiquitous RNA processing protein, to be a promoter of interferon inflammatory signaling in murine infection models. We used a knockout model to show that this protein impacts mouse response to ligands (LPS) and pathogens (Salmonella) and that it mice that lack this protein are more susceptible to infection. We highlight the novel and integral role HNRNPA2B1 plays as a novel modulator of the inflammatory cascade and a major contributor to the innate immune response to stimulus.

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