Thomas and colleagues describe how multiple SARS-CoV-2 antigen exposures, including mRNA vaccine boosters, primary infection and breakthrough infection, shape T cell immunity.

Schumacher and colleagues have designed a reporter system that allows in vivo tracking of replicative history over many cell generations. Using this system to study acute T cell responses, they uncover substantial diversity in past division of central memory CD8⁺ T cells and its link to cell state and recall potential.

A new genetic ‘recorder’ of long-term cell proliferation revealed substantial heterogeneity in the division history of central memory CD8⁺ T cells. Importantly, the extent of past proliferation was related to distinct transcriptional features and re-expansion potential, highlighting an unappreciated division of labor within the central memory T cell pool.

Colonna and colleagues present a genome-wide characterization of DNA methylation and hydroxymethylation in innate lymphocytes and identify differentially methylated and hydroxymethylated regions between NK cells, ILC2s and ILC3s.

Schumacher and colleagues have designed a reporter system that allows in vivo tracking of replicative history over many cell generations. Using this system to study acute T cell responses, they uncover substantial diversity in past division of central memory CD8⁺ T cells and its link to cell state and recall potential.

Thomas and colleagues describe how multiple SARS-CoV-2 antigen exposures, including mRNA vaccine boosters, primary infection and breakthrough infection, shape T cell immunity.

Tussiwand and colleagues show that an uncommitted precursor expressing the lymphoid-specific factor TdT generates a large fraction of myeloid and a substantial fraction of erythro-megakaryocyte cells.

Nie et al. show that the transcription factor LRF, by upregulating expression of the integrin gene Itgb7, imprints thymic precursors of CD8αα⁺ intraepithelial lymphocytes for eventual seeding of the gut tissues.

Rinkevich and colleagues show that preexisting matrix is transferred by neutrophils across organs into injured sites in a manner dependent on integrin activation.

Fabry and colleagues show that cribriform plate-resident lymphatic endothelial cells respond to neuroinflammatory signals by inducing functional changes that enhance antigen capture and presentation from the cerebrospinal fluid and promote leukocyte interactions within the central nervous system.