Abstract

IN the mouse the injection of bacterial lipopolysaccharide (LPS) results in the appearance of very large numbers of IgM globulin-secreting cells1. Furthermore, it has been shown that LPS induces B lymphocytes, both in vivo2,3 and in vitro4–6 to secrete IgM antibodies to a wide range of seemingly unrelated antigens. It was reported recently that about 8% of all IgM globulin-secreting cells arising as a consequence of LPS injection into CBA mice secrete an antibody-like molecule with specificity for a heterospecific (bovine) IgG (BIG) molecule1. It was suggested that such IgM molecules were reminiscent of a rheumatoid factor, although at that time plaque-forming cells (PFC) had not been demonstrated using mouse IgG (MIG) as the target antigen. I have now been able to demonstrate the presence of auto-(anti-MIG)-antibody-forming cells. About half (35–75%) of all IgM-secreting cells appearing after both mitogen and immunogen injection into mice produce IgM globulin which is not specific for the inducing immunogen, but which does have specificity for self-IgG. The description by Steel and Cunningham7 of a large proportion of IgM-PFC having specificity for normally hidden (syngeneic) erythrocyte antigens, supports a view that a majority of both mitogen and immunogen stimulated IgM-PFC are producing auto-antibodies. Although a mouse rheumatoid-like IgM with binding activity against antigen-bound (syngeneic) IgG was described previously8, until now attempts to develop a haemolytic plaque assay for autologous mouse M-anti-G have failed. After unsuccessful attempts involving various forms of mouse IgG, partially denatured mouse IgG and also a procedure used successfully in the rabbit9, a successful method has been developed. An account of some of the results from experiments using this methodology is presented here.

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