title: CD5+ B cells in autoimmune disease and lymphoid malignancy.
abstract: Evidence is accumulating that CD5+ B cells belong to a developmental lineage distinct from that of conventional B cells and mainly participate in natural immunity. They have attracted attention because of their involvement in autoimmunity and lymphoid malignancy in both mice and humans. Patients with rheumatoid arthritis and Sjögren's syndrome were found to show a striking increase in the number of CD5+ B cells. B cell-chronic lymphocytic leukemia cells frequently express CD5. However, there are arguments against the role for CD5+ B cells in autoimmune disease, particularly in murine and human systemic lupus erythematosus (SLE). Whereas most IgM anti-DNA antibodies are produced by CD5+ B cells, high-affinity, pathogenic IgG antibodies are produced mainly by CD5- B cells. Either of two possibilities can explain the failure of CD5 expression of B cells responsible for producing IgG anti-DNA antibodies: either the cells are conventional B cells or the cells are CD5+ B cells that lack CD5 expression. In studies using SLE-prone NZB x NZW F1 mice and their H-2-congenic progeny, we discussed herein the possibility that CD5+ B lineage cells are also responsible for the pathogenic IgG autoantibody production by phenotypic switching from CD5+ to CD5-, probably under a particular genetic background. A line of H-2-congenic NZB x NZW F1 progeny failed to produce IgG anti-DNA antibodies, but in turn, showed a marked clonal proliferation of CD5+ B cells. Thus, it appears that genetically determined signals for either proliferation or differentiation would lead CD5+ B cells to cause distinct disease, i.e., autoimmune disease or lymphoid malignancy. Further studies using H-2-congenic New Zealand mice may provide insights into the correlation between autoimmunity and related lymphoid malignancy.
authors.affiliation: Department of Pathology, Juntendo University School of Medicine, Tokyo, Japan.
authors.forename: T
authors.initials: T
authors.lastname: Shirai
authors.forename: S
authors.initials: S
authors.lastname: Hirose
authors.forename: T
authors.initials: T
authors.lastname: Okada
authors.forename: H
authors.initials: H
authors.lastname: Nishimura
mesh_terms: D000818:Animals; D015703:Antigens, CD / Q000032:analysis*; D000943:Antigens, Differentiation / Q000032:analysis*; D001327:Autoimmune Diseases / Q000276:immunology*; D001402:B-Lymphocytes / Q000276:immunology*; D018956:CD5 Antigens; D006801:Humans; D007113:Immunity, Innate; D007938:Leukemia / Q000276:immunology*; D008223:Lymphoma / Q000276:immunology*; D051379:Mice; D008814:Mice, Inbred NZB / Q000235:genetics / Q000276:immunology*
chemical_list: D015703:Antigens, CD; D000943:Antigens, Differentiation; D018956:CD5 Antigens