title: Requirement of IL-5 for induction of autoimmune hemolytic anemia in anti-red blood cell autoantibody transgenic mice.
abstract: 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 alpha chain-deficient HL (IL-5Ralpha-/- x HL) mice generated by the cross between IL-5Ralpha-/- and HL mice. In IL-5Ralpha-/- 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-5Ralpha-/- x HL mice. We also used in vivo 5-bromo-2'-deoxyuridine labeling to estimate the proliferation of B-1 cells in IL-5Ralpha-/- mice. The absence of IL-5Ralpha 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-5Ralpha-/- 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.
authors.affiliation: Department of Medical Chemistry, Faculty of Medicine, Kyoto University, Sakyo-ku, Yoshida, Kyoto 606-8501, Japan.
authors.forename: T
authors.initials: T
authors.lastname: Sakiyama
authors.forename: K
authors.initials: K
authors.lastname: Ikuta
authors.forename: S
authors.initials: S
authors.lastname: Nisitani
authors.forename: K
authors.initials: K
authors.lastname: Takatsu
authors.forename: T
authors.initials: T
authors.lastname: Honjo
mesh_terms: D000744:Anemia, Hemolytic, Autoimmune / Q000235:genetics* / Q000276:immunology*; D000818:Animals; D001323:Autoantibodies / Q000235:genetics*; D001402:B-Lymphocytes / Q000276:immunology / Q000378:metabolism; D004912:Erythrocytes / Q000276:immunology*; D016753:Interleukin-10 / Q000494:pharmacology; D015848:Interleukin-5 / Q000276:immunology / Q000502:physiology*; D008070:Lipopolysaccharides / Q000494:pharmacology; D051379:Mice; D018345:Mice, Knockout; D008822:Mice, Transgenic; D018123:Receptors, Interleukin / Q000172:deficiency / Q000235:genetics / Q000502:physiology; D053649:Receptors, Interleukin-5
chemical_list: D001323:Autoantibodies; D015848:Interleukin-5; D008070:Lipopolysaccharides; D018123:Receptors, Interleukin; D053649:Receptors, Interleukin-5; D016753:Interleukin-10