Masato Ogishi

This paper develops TGF-β agonists targeting specific T and B cells to selectively suppress pathogenic immune responses in autoimmune and inflammatory diseases.

Homozygosity for hypomorphic IL23R variants (G149R, G300V, R381Q) partly impairs IL-23-dependent IFN-γ production in patient cells; with L372F (effect inferred), they are enriched in tuberculosis, not MSMD or CMC patients.

The paper designs proteins with controlled dissociation rates by introducing strained excited states, enabling rapid cytokine receptor dissociation.

The paper identifies clonal inflammatory microglia as a cause of neurodegeneration in LCH and ECD, showing their association with neuronal loss and suggesting CSF1R inhibitors as a therapeutic option.

The paper identifies microglia-specific somatic clones with pathogenic variants in Alzheimer's Disease patients that drive neuro-inflammation through the MAPK pathway.

The paper introduces iMUBAC, a framework for integrating multi-batch cytometry data to identify cell types and detect immunophenotype abnormalities across datasets.

This paper introduces a computational framework to prioritize etiologically relevant T cell epitopes in autoimmune diseases using HLA allele-disease risk associations and a differential presentation index.