International Immunology, Vol. 11, No. 6, 995-1000,
June 1999
© 1999 Japanese Society for Immunology
Requirement of IL-5 for induction of autoimmune hemolytic anemia in anti-red blood cell autoantibody transgenic mice
Department of Medical Chemistry, Faculty of Medicine, Kyoto University, Sakyo-ku, Yoshida, Kyoto 606-8501, Japan
1 Department of Immunology, Institute of Medical Science, University of Tokyo, 4-6-1 Shirokanedai, Minato-ku, Tokyo 108, Japan
Correspondence to: T. Honjo
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 
chain-deficient HL (IL-5R–/– x HL) mice generated by the cross between IL-5R–/– and HL mice. In IL-5R–/– x 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-5R–/– x HL mice. We also used in vivo 5-bromo-2'-deoxyuridine labeling to estimate the proliferation of B-1 cells in IL-5R–/– mice. The absence of IL-5R 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-5R–/– 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.
Keywords: autoimmune hemolytic anemia, IL-5
2 Present address: Kagoshima Medical Association Hospital, 7-1 Kamoikeshinmachi, Kagoshima 890-0064, Japan
3 Present address: Howard Hughes Medical Institute University of California, Los Angeles, 5-721 MRL, 675 Circle Drive South, Box 951662, Los Angeles, CA 90095-1662, USA
Transmitting editor: T. Watanabe
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