Elucidating widespread and tissue-specific biological process alterations after myocardial infaction in metabolically active tissues using systems biology approaches.

Malaria remodels the spleen to imprint tolerance and reduce pathology in subsequent infections.

Type I IFN is a key determinant of pathogenic neutrophil activity and drives tissue pathology through modulation of IL-18 levels during genital HSV infection.

LPS pre-exposure is tissue protective during a subsequent lethal E. coli peritonitis by long-term modulation the bone marrow B-cell and neutrophil pool which affects neutrophil tissue damaging properties and therapeutic activation of Cxcr4 promotes tissue damage control during sepsis.

A computational framework allows the unsupervised analysis of samples from single cell data across conditions, inference of multicellular programs associated with disease, and meta-analysis of independent patient cohorts.

Data exploring host and parasite signatures in the peripheral blood indicate that total parasite biomass is a better predictor of P. vivax-induced host responses and pathogenesis than peripheral parasitemia.

The secreted toxin mycolactone has severe effects on the cells lining blood vessels that will play a critical role in the development of swelling in Buruli ulcer disease.

An innate immune system signaling pathway in planarians has a dual role: it enhances apoptosis during bacterial infection, but represses apoptosis during tissue regeneration in the absence of infection.

Pathogen-specific CTLs are programmed to provide customized responses against infection, by inflammatory molecules that promote localization in peripheral and lymphoid tissues using alternative signaling mechanisms.

Exchange of the I domain in the Plasmodium surface protein TRAP against evolutionary distant I domains rescues infectivity of sporozoites.