Location, infection history, antigen persistence shape the phenotype of tissue-resident T cells (Trm), challenging the idea of a universal framework for Trm identity across organs and diseases.
High/low antigen immunogenicity may add another layer...

@cp-immunity.bsky.social

tinyurl.com/49dkc3j7

A commensal bacterium triggers systemic antibody responses via skin lymphoid structures and can be engineered as a topical vaccine – great therapeutic potential!

Two studies in @nature.com.web.brid.gy by the Fischbach and Belkaid labs

tinyurl.com/5yahn47t
tinyurl.com/4n4btxap

Link to publication and short graphical abstract below!
www.cell.com/immunity/ful...

...aaaand, we even made the cover at Immunity!
Big thanks to all the funding agencies, collaborators, mentors and friends who made this paper possible!

This allowed recovered mice to be better at combatting secondary influenza A virus infection - an effect that seemed to be solely mediated by recovered alveolar macrophages, independent of SARS2-memory T cells!

We found that alveolar macrophages retain epigenetic remodeling post COVID-19 that allows them to hyper-induce antiviral genes after encountering a secondary viral pathogen

How do past viral infections influence future viral diseases? We found that SARS-CoV-2 recovery protected from severe influenza A virus disease. But how come? There seemed to be some antigen-independent immunological memory going on..

Paper at Immunity: www.sciencedirect.com/science/arti...

Chronic autoimmunity rewires metabolism in progenitors, correlating with innate immune memory formation in macrophages that increases antibacterial activity but might also aggravate autoimmune diseases?
shorturl.at/SZ1Ww

#CellStemCell

This allowed recovered mice to be better at combatting secondary influenza A virus infection - an effect that seemed to be solely mediated by recovered alveolar macrophages, independent of SARS2-memory T cells!

We found that alveolar macrophages retain epigenetic remodeling post COVID-19 that allows them to hyper-induce antiviral genes after encountering a secondary viral pathogen