Humoral immunity articles from across Nature Portfolio

Computational methods can be used to find potent neutralizing antibodies against viruses such as SARS-CoV-2. Here the authors use an AI method to landscape antibodies, predict specificity and antibody-antigen structure, pick out potent neutralizers and show that these antibodies are protective against SARS-CoV-2 challenge in mice models.

The rapid evolution of SARS-CoV-2 challenges antibody therapeutics, but glycan-masked antigens enable isolation of class 3 monoclonal antibodies that potently neutralize diverse Omicron variants and reveal cross-reactive epitopes.

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

B cell receptors (BCR) are the membrane-bound counterparts of antibodies, and the role of N-linked glycans in their functions are much less known than that of circulating immunoglobulins. Here authors study the site-specific glycosylation profiles of all 4 N-linked glycosylation sites of human Igµ BCRs expressed in naïve and memory B cells and conclude that these show high level of conservation across development and don’t contribute to differences in their expression and function.

Immune imprinting narrows the vaccine recall response towards dominant epitopes but protection against rapidly evolving viruses is enhanced if the breadth of responses is preserved. Here authors show in a ferret model that introducing optimized antigenic variation between prime and boost vaccines diversify the targeted epitopes and thus broadens immunity in a ferret model of influenza vaccination.

Nechanitzky et al. examine the cell-intrinsic role of choline acetyltransferase (ChAT)-expressing B cells in germinal center immune responses.

Zhu et al. report in Immunity that ketogenesis resulting from intermittent fasting causes the downregulation of CXCR4 expression on plasma cells, triggering their egress from the bone marrow and impaired humoral immunity.

A preprint by Yan et al. reports that local antibody production in germinal centres contributes to negative feedback on low-affinity B cells that target the same epitope.

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.

A complex of the NF-κB family member p52 and the transcription factor ETS1 is required for B cell germinal center responses to T cell-dependent immunization and for IgE-dependent allergic responses.