Protective B Cell Responses to Flu—No Fluke!

Abstract

The mechanisms regulating the induction and maintenance of B lymphocytes have been delineated extensively in immunization studies using proteins and hapten-carrier systems. Increasing evidence suggests, however, that the regulation of B cell responses induced by infections is far more complex. Here we review the current understanding of B cell responses induced following infection with influenza virus, a small RNA virus that causes “the flu”. Notably, the rapidly induced, highly protective and long-lived humoral response to this virus is contributed by multiple B cell subsets, each generating qualitatively distinct respiratory tract and systemic responses. Some B cell subsets provide extensive cross-protection against variants of the ever-mutating virus and each is regulated by the quality and magnitude of infection-induced innate immune signals. Knowledge gained from the analysis of such highly protective humoral response might provide a blueprint for successful vaccines and vaccination approaches.

Adjuvant solution for pandemic influenza vaccine production

“…Another distinguishing feature of GLA-SE is its ability to amplify a Th1 CD4 T-cell response; animals immunized with GLA-SE produced >30-fold more IFN-γ + CD4 T cells than the number of IL-5 + CD4 T cells stimulated with SE, which led to a significant IgG1 to IgG2c shift in antibody expression. Mechanistically, antibody responses are critical for anti-influenza protection (23,24). Consistent with this fact, we showed that B cells were required for rH5-induced protection and that conditions that increased antibody production improved recovery from infection.…”

Evaluating the case for trivalent or quadrivalent influenza vaccines

“…This facilitates viral evasion of the longterm control of infection by neutralising antibodies. 15 With antigenic drift, although the variant differs from the parent virus, this difference is sufficiently small that existing antibody to the parent virus is able to provide some, albeit incomplete protection. Nevertheless, the novel variant now becomes the predominant strain.…”

Expression of plasma cell alloantigen 1 defines layered development of B-1a B-cell subsets with distinct innate-like functions

“…Previous studies showed that peritoneal B-1a cells can migrate to the spleen (36,37) and that those present in the pleural cavity can migrate to mediastinal lymph nodes (38). To determine whether the peritoneal B-1a subsets differ in their migratory potential, we adoptively transferred equal numbers of sort-purified subsets i.p.…”