Sepsis leads to lasting changes in the composition of the pre-existing memory CD8 T cell compartment leading to altered localization, changes in their transcriptional landscape and chromatin accessibility, differential function, and reduced capacity to control infection.

Altered lymphocyte dynamics after hematopoietic stem cell transplantation cannot solely be explained by low lymphocyte numbers.

The p21-activated kinase 2 (Pak2) is an essential regulator that governs the actin cytoskeleton-dependent signaling to ensure normal thymocyte development, maturation and egress.

Naive CD4 and CD8 T cells in mice increase their survival capacity with age, but their numbers are not homeostatically regulated.

Autophagy is required for CD8⁺ T cell memory formation; in aged individuals autophagy levels are diminished, and increasing autophagy enhances their CD8⁺ T cell responses.

Sepsis-induced numerical loss of naive autoantigen-specific CD4 T cells reduces host capacity to develop autoimmune immune disease, thereby demonstrating an intriguing relationship between infection and autoimmune disease.

Human CRACR2A insufficiency underlies progressive loss of immune competence by uncoupling TCR activation from Ca2+ and MAPK signaling and should be included within the group of combined immunodeficiency disorders in the IEI classification.

Homeostatic innate lymphoid cell abundance, adjusted for age and sex, correlates inversely with COVID-19 severity in adults and children.

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.

Remdesivir is a promising treatment modality to reduce 30 day all-cause mortality.