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B cell differentiation and memory are controlled by the transmembrane activator and CAML interactor (TACI), a receptor encoded by  TNFRSF13B .  TNFRSF13B  mutations are frequently found in common variable immunodeficiency (CVID) and in IgA -deficiency; yet, ~98% of those with mutant  TNFRSF13B  are healthy. Indeed,  TNFRSF13B  is among the 5% most polymorphic genes in man. Other mammals evidence polymorphism at comparable loci. We hypothesize that  TNFRSF13B  diversity might promote rather than detract from well-being by controlling key elements of innate immunity. We shall discuss how extraordinary diversity of  TNFRSF13B  could have evolved and persisted across diverse species of mammals by controlling innate and adaptive B cell responses in apparently paradoxical ways.

TNFRSF13B Diversification Fueled by B Cell Responses to Environmental Challenges—A Hypothesis