title: RP105-lacking B cells from lupus patients are responsible for the production of immunoglobulins and autoantibodies.
abstract: OBJECTIVE
  We previously reported that B cells lacking the RP105 molecule, which proved to be highly activated B cells, are increased in the peripheral blood of patients with systemic lupus erythematosus (SLE). In the present study, we attempted to determine whether RP105-negative B cells obtained from SLE patients would be capable of producing autoantibodies as well as immunoglobulins.
  
  
  METHODS
  RP105-positive and RP105-negative B cells, sorted by cell sorter, were cultured for 5 days without stimulation, or were stimulated with Staphylococcus aureus Cowan 1 strain (SAC) or recombinant interleukin-6 (IL-6). For the assay of autoantibodies, RP105-positive and RP105-negative B cells were cultured separately for 10 days with anti-CD3 antibody-stimulated T cells. The production of immunoglobulins and autoantibodies was determined by enzyme-linked immunosorbent assay.
  
  
  RESULTS
  We demonstrated that RP105-negative B cells, but not RP105-positive B cells, obtained from SLE patients could spontaneously produce IgG and IgM in vitro until day 5. SAC and IL-6 enhanced production of IgG and IgM by RP105-negative B cells but failed to induce such production by RP105-positive B cells. The latter cells, however, when cocultured with activated T cells in the presence of IL-10, produced IgG, although the amount was very small compared with that produced by RP105-negative B cells. Most important, under these conditions, anti-double-stranded DNA antibodies were produced only by the RP105-negative B cells obtained from SLE patients.
  
  
  CONCLUSIONS
  These data indicate that RP105-negative B cells, constituting a subset of B cells in SLE patients, are highly activated and may be responsible for the production of autoantibodies as well as polyclonal immunoglobulins.
authors.affiliation: Saga Medical School, Saga, Japan. Kikuchin@intmed1.med.kyushu-u.ac.jp
authors.forename: Yuji
authors.initials: Y
authors.lastname: Kikuchi
authors.forename: Syuichi
authors.initials: S
authors.lastname: Koarada
authors.forename: Yoshifumi
authors.initials: Y
authors.lastname: Tada
authors.forename: Osamu
authors.initials: O
authors.lastname: Ushiyama
authors.forename: Fumitaka
authors.initials: F
authors.lastname: Morito
authors.forename: Noriaki
authors.initials: N
authors.lastname: Suzuki
authors.forename: Akihide
authors.initials: A
authors.lastname: Ohta
authors.forename: Kensuke
authors.initials: K
authors.lastname: Miyake
authors.forename: Masao
authors.initials: M
authors.lastname: Kimoto
authors.forename: Takahiko
authors.initials: T
authors.lastname: Horiuchi
authors.forename: Kohei
authors.initials: K
authors.lastname: Nagasawa
mesh_terms: D000293:Adolescent; D000328:Adult; D000368:Aged; D000974:Antibodies, Antinuclear / Q000096:biosynthesis; D015703:Antigens, CD / Q000378:metabolism*; D001323:Autoantibodies / Q000096:biosynthesis*; D001402:B-Lymphocytes / Q000382:microbiology / Q000502:physiology*; D004247:DNA / Q000276:immunology; D006801:Humans; D007074:Immunoglobulin G / Q000096:biosynthesis; D007075:Immunoglobulin M / Q000096:biosynthesis; D007136:Immunoglobulins / Q000096:biosynthesis*; D015850:Interleukin-6 / Q000494:pharmacology; D008180:Lupus Erythematosus, Systemic / Q000378:metabolism*; D011994:Recombinant Proteins / Q000494:pharmacology; D013211:Staphylococcus aureus / Q000502:physiology
chemical_list: D000974:Antibodies, Antinuclear; D015703:Antigens, CD; D001323:Autoantibodies; C092722:CD180 protein, human; D007074:Immunoglobulin G; D007075:Immunoglobulin M; D007136:Immunoglobulins; D015850:Interleukin-6; D011994:Recombinant Proteins; D004247:DNA