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Lymph node lymphocytes from rats immunized with a guinea pig encephalitogenic protein (GEProt) were incubated in vitro with the immunizing antigen in a serum-free medium. They released a factor which had the property to combine with IgG antibodies complexed with antigen, but not IgM antibodies, inducing hemagglutination of IgG-sensitized erythrocytes and protecting IgG-sensitized erythrocytes, but not IgM-sensitized erythrocytes from complement-induced hemolysis. A similar activity was found in supernatants from mixed leukocyte cultures between allogenic mouse strains. This factor was named immunoglobulin-binding factor (IBF). IBF was separated in rat from migration inhibitory factor, blastogenic factor, and lymphotoxin upon column fractionation techniques. IBF activity was found in fractions of about 150,000 m.w. and with a pH of about 6.30.

An immunoglobulin-binding factor (IBF) has been detected in incubation supernatants from cortisone-resistant normal thymus cells and educated thymus cells but not untreated normal thymus cells. IBF is synthesized by the cells under test, since, for instance, it could not be detected in supernatants from cells incubated in the presence of inhibitors of protein synthesis. Moreover, IBF has been detected in supernatants from very small numbers of highly purified educated T cells, strongly suggesting that non-T cells are not involved in its production. IBF activity has also been found at the surface of about 1% of cortisone-resistant normal thymus cells and 4%–19% of educated thymus cells. Both cell surface and supernatant IBF have a specificity for the Fc region of immunoglobulins G. The existence of immunoglobulin-binding factors at the surface of some T cells and in supernatants from T cells (1) should be taken into consideration for the interpretation of results of experiments investigating immunoglobulin production by T cells, and (2) may well be relevant to fundamental mechanisms in T and non-T cell functions and interactions.

BOTH serological and cell-mediated immunological reactions of the primary host against his own tumour cells have been demonstrated in an increasing number of experimental tumours1; promising results have also been obtained with human tumour cells as antigens and patient's own serum as the source of antibody2–5, and some experiments suggest that cell mediated immune reactions may also be involved6–8. Stimulation of lymphocytes in mixed cultures in vitro is a possible method for the detection of antigenic differences between two types of cells9. We have observed an increase of thymidine incorporation in vitro into lymphocytes from the remission period, when cultivated in the presence of mitomycin C treated autologous leukaemic leucoblasts. The cells were from ten patients with acute leukaemia, nine acute lymphoblastic leukaemias and one acute myelo-blastic leukaemia with hyperleucocytosis (over 50,000 leucocytes per mm3).

“Sensitized” lymphocytes from rats, mice, and human beings were cultured in the presence of the immunizing antigen for 24 hr in a serum-free system. Under these conditions the lymphocytes released a soluble factor which prevented the combination of C1 with antigen-IgG complexes. This factor prevented the fixation of guinea-pig C1, as well as the fixation of rat, human and hamster C1. The fixation of C1 on antigen-IgM complexes was not blocked. After purification of this factor from rat lymphocytes, it was shown to have a m.w. of about 150,000, a sedimentation constant of 7S, an electrophoretic mobility of a γ-globulin and an isoelectric point of 6.30. It was remarkably stable both at 56°C and over a wide range of pH values. When used either in a soluble purified state or as a complex with antigen-IgG antibody it did not combine with non-aggregated IgG in the fluid phase, nor did it destroy C1 in serum.