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IL-5, IL-10 and lipopolysaccharide (LPS) are known to activate B-1 cells in vivo in normal mice and anti-red blood cell autoantibody transgenic mice (HL mice). To assess the exact role of IL-5 in proliferation and activation of peritoneal B-1 cells, we analyzed IL-5 receptor α chain-deficient HL (IL-5Rα–/– × HL) mice generated by the cross between IL-5Rα–/– and HL mice. In IL-5Rα–/– × HL mice, Ig-producing B-1 cells in the peritoneal cavity were negligible, although the total number of B-1 cells in the peritoneal cavity were as many as 30% of that in HL mice. Moreover, LPS- or IL-10-induced differentiation of B-1 cells into antibody-producing cells was severely impaired in IL-5Rα–/– × HL mice. We also used in vivo 5-bromo-2′-deoxyuridine labeling to estimate the proliferation of B-1 cells in IL-5Rα–/– mice. The absence of IL-5Rα did not affect spontaneous proliferation of peritoneal B-1 cells. However, induced proliferation of peritoreal B-1 cells by oral administration of LPS was markedly impaired in IL-5Rα–/– mice. These results suggest that IL-5 is required for activation-associated proliferation of B-1 cells but not for their spontaneous proliferation and support the idea that IL-5 plays an important role on the induction of autoantibody production from B-1 cells. [ABSTRACT FROM PUBLISHER]