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Rheumatoid Synovial Fluid Reconstitutes the B‐Cell Defect in CBA/N Mice
Author(s) -
RIDDERSTAD A.,
ABEDIVALUGERDI M.,
STRÖM H.,
MÖLLER G.,
MÖLLER E.
Publication year - 1989
Publication title -
scandinavian journal of immunology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.934
H-Index - 88
eISSN - 1365-3083
pISSN - 0300-9475
DOI - 10.1111/j.1365-3083.1989.tb02485.x
Subject(s) - lipopolysaccharide , spleen , immunology , antibody , secretion , b cell , in vitro , biology , b 1 cell , antigen , microbiology and biotechnology , immune system , chemistry , t cell , endocrinology , antigen presenting cell , biochemistry
Synovial fluid from patients with rheumatoid arthritis (RA‐SF) contains a biological activity which can replace T cells for activation of antibody secretion in human blood lymphoid cells and which can also induce the selective differentiation of IgG2b‐secreting cells in lipopolysaccharide (LPS)‐pre‐activated mouse spleen cells. The B‐cell activity of this factor was studied in CBA/N mice which have an X‐linked B‐cell immunodeficiency which manifests itself as a defective humoral response to certain thymus‐independent antigens (TI‐2). RA‐SF has now been shown to reconstitute partly the B‐cell deficiency in CBA/N splenic B cells in vitro Addition of RA‐SF to LPS‐pretreated cell cultures results in IgG2b secretion in CBA/N spleen cells as well. In contrast to cells from normal CBA mice, cells from CBA/N mice cannot respond to interleukin 4 (IL‐4) after addition of LPS with production of IgG1 antibodies in vitro. However, the addition of RA‐SF completely restores a normal IL‐4‐induced IgG1 response. No other biologically active factors have been shown to allow the production of IgG antibody producing cells in CBA/N splenic B cells. It is postulated that the xid immunodeficiency could be the result of a deficient production of a biological activity which is abundant in RA‐SF.