Interestingly, although redundant for active resistance during 4X infection in WT mice, the development of atypical and/or regulatory CD11c+, PDCA-1+ and PDL-1+ B cell populations, as well as CD138+ and CD80+ populations, were abrogated in 4X IgMi mice (Figure 6D), indicating that infection-induced development of atypical B cell populations during malaria was dependent upon secreted antibody. This evidence concerns the gene ITGAX and infection.