Immunological memory articles from across Nature Portfolio

Oakes et al., evaluated cellular and humoral immune responses after influenza vaccinations in adults. Vaccination elicited comparable serologic responses; however, adults 65 years old and over had reduced cellular immune responses, and single-cell RNA sequence analysis revealed that they had attenuated IFN transcriptional signatures in T-helper and myeloid cell subsets.

Lin et al. investigate the immune response in severely ill H7N9 patients and its link to early-life influenza imprinting. They find that individuals first exposed to H2N2 develop faster, higher-avidity cross-reactive antibodies and tend to experience less severe illness.

In a mouse model that mimics Sudan virus infection, a deadly relative of Ebola virus, vaccine protection depends on virus-specific CD4 T cells that coordinate antiviral defenses, even in the absence of neutralizing antibodies.

Imprinting by influenza viruses can cause a deleterious shift of nearly the entire memory recall response against key, conserved epitopes.

A preprint by Villazala-Merino et al. shows that allergen-specific memory B cells must re-enter germinal centres to differentiate into IgE-producing plasma cells, which occurs in lymph nodes but not at barrier sites.

We identified T cell receptors (TCRs) targeting antigenic peptides that contain a shared β-catenin mutation (CTNNB1^S37F) presented on common human leukocyte antigen alleles. TCR-engineered T cells eliminated patient-derived tumors and prevented relapse in vivo in mice, highlighting a strategy to exploit public neoantigens for TCR-based immunotherapy in solid cancers.

TGFβ-mediated signals enable CD8⁺ T cells to establish tissue-residence. IL-4 and PD-1 are each connected to TGFβ signaling to regulate the formation of CD8⁺ T cell tissue residence in skin.