In mice, both CD4 T-cell-independent and -dependent antibody responses contribute to the control of infl uenza virus infection (27, 28) . Although antibodies appear to facilitate the recovery from infl uenza infection, it is generally believed that B cells cannot produce neutralizing, isotypeswitched, infl uenza-specifi c antibodies in the absence of CD4 T-cell help (29, 30) . However, other data clearly demonstrate that B cells can also produce anti-infl uenza IgA, IgM, and IgG responses independent of CD4 helper T cells (27, 31) . A non-antigen-specifi c bystander response driven by activated CD4 T cells specifi c for heterologous antigen may contribute to so-called heterosubtypic immunity (8) (9) (10) 12) . However, the ability of infl uenza virus infection to promote B-cell activation and differentiation into shortlived, isotype-switched, antibody-secreting cells may result from a combination of B-cell receptor hypercross-linking, engagement of toll-like receptors, production of cytokines, as well as triggering of innate immunity.