title: Heterogeneous responses of B-cell tumours to anti-Ig and anti-idiotypic antibodies.
abstract: Anti-Ig antibodies can have two opposing effects on B-cell proliferation, resulting either in stimulation or inhibition. We have examined the proliferative response of 30 B-cell tumours to anti-Ig in the presence and absence of B-cell growth factor. Three reaction patterns were observed. In 12 cases a dose-dependent synergism between anti-Ig and B-cell growth factor was present in the induction of proliferation, in ten cases anti-Ig did not induce any response, and in eight cases anti-Ig suppressed the B-cell growth factor (BCGF)-induced proliferation. Similar responses to anti-Ig were found in the absence of BCGF. When these B-cell tumours were typed for expression of Ig isotypes, HLA class II antigens, several B-cell markers, activation markers, complement receptors, Fc receptors, cell size, and cell cycle phase, no correlation could be found with the proliferative response of these tumour B cells to anti-Ig. T cells or T-cell factors were not involved, because T-cell depletion did not change the tumour B-cell proliferative response to incubation with anti-Ig. The observed inhibition of proliferation did not correlate with the expression of Fc receptors, indicating the involvement of suppressor mechanisms other than the cross-linking of Fc receptors with surface immunoglobulins. Tumour B cells, for which monoclonal anti-idiotypic antibodies (MoAb anti-id) were available, responded to MoAb anti-id in the same way as they did to anti-Ig. In view of the treatment of B-cell malignancies with MoAb anti-id, the question of whether these responses in vitro correlate with in vivo clinical outcome of anti-id therapy is of interest. So far our data show that the proliferative response of B-cell tumours to anti-Ig or MoAb anti-id is heterogeneous and cannot be linked to phenotype, is T cell-independent, and is most likely an intrinsic property of the malignant cell.
authors.affiliation: Department of Nephrology, University Hospital, Nijmegen, The Netherlands.
authors.forename: W A
authors.initials: WA
authors.lastname: Allebes
authors.forename: R H
authors.initials: RH
authors.lastname: Wetzels
authors.forename: P J
authors.initials: PJ
authors.lastname: Capel
mesh_terms: D000888:Antibodies, Anti-Idiotypic / Q000502:physiology*; D000911:Antibodies, Monoclonal / Q000502:physiology*; D000954:Antigens, Surface / Q000032:analysis / Q000276:immunology; D000955:Antigens, T-Independent / Q000276:immunology; D001402:B-Lymphocytes / Q000145:classification / Q000276:immunology*; D004306:Dose-Response Relationship, Immunologic; D006801:Humans; D007130:Immunoglobulin Idiotypes / Q000276:immunology*; D007945:Leukemia, Lymphoid / Q000276:immunology; D008213:Lymphocyte Activation; D008223:Lymphoma / Q000276:immunology; D010641:Phenotype; D014407:Tumor Cells, Cultured / Q000276:immunology*
chemical_list: D000888:Antibodies, Anti-Idiotypic; D000911:Antibodies, Monoclonal; D000954:Antigens, Surface; D000955:Antigens, T-Independent; D007130:Immunoglobulin Idiotypes