Gajanan Dattatray Katkar

The paper identifies GIV as a macrophage checkpoint suppressing reverse cholesterol transport and shows its inhibition restores cholesterol efflux, reducing plaque burden and systemic lipid overload.

This paper identifies two stromal states in IBD that predict clinical outcomes and shows that targeting one state can reverse disease pathology.

This paper identifies GIV as a macrophage-intrinsic factor that controls PD1 endocytosis, determining durable response versus hyperprogressive disease to PD1 blockade.

This paper identifies a host-encoded toggle switch involving NOD2 and GIV that controls cAMP levels in macrophages, converting tolerant cells into microbicidal machines to restore microbial clearance and gut barrier integrity.

The paper identifies niColAMs as critical for IBD recovery and shows GIV-NOD2 interaction is essential for microbial sensing and gut homeostasis.

The paper identifies a 338-gene signature of macrophage reactivity and tolerance that predicts disease outcomes across diverse conditions and species.

The paper uses BoNE to identify dual PPARα/γ agonism as a therapeutic strategy for IBD, validated in preclinical models and patient-derived cells.

The paper identifies a conserved 166-gene host immune signature across viral pandemics, with a 20-gene subset predicting disease severity and guiding therapeutic strategies.