Complement Receptor Subtypes C3b and C3d in Lymphatic Tissue and Follicular Lymphoma

Abstract

Summary.-To substantiate the origin of follicular (nodular) lymphoma cells from germinal-centre cells, the lymphoma cells from 7 patients with follicular lymphoma and from 9 tonsils and 2 lymph nodes were studied for the presence and distribution of complement-receptor subtypes (i.e., the receptors for C3b and C3d). It was found that erythrocytes coated with antibodies and C3d (EAC3d) adhered exclusively to germinal centres, whereas erythrocytes coated with antibodies and C3b (EAC3b) adhered to germinal centres and in many instances to the regions between them. These findings indicate that germinal-centre cells bear both complementreceptor subtypes and that the B cells of the interfollicular area, which belong at least in part to the precursors of plasma cells, bear only a receptor for C3b. In frozen sections of follicular lymphomas, a similar distribution of complementreceptor subtypes was observed; EAC3d was bound exclusively to the neoplastic nodules, and EAC3b adhered to the neoplastic nodules and adjacent paranodular tissue. Receptor studies on suspended cells of both normal tonsils and follicular lymphomas revealed a slight predominance of EAC3d+ cells or equal numbers of EAC3b+ and EAC3d+ cells. The complete congruence in the expression and Idistribution of complement-receptor subtypes between tissues from follicular lymphomas and those from normal and hyperplastic tonsils or lymph nodes suggests that follicular lymphoma represents the neoplastic counterpart of the reactive germinal centre.

Morphological and immunological definition of a malignant lymphoma derived from germinal-centre cells with cleaved nuclei (centrocytes)

“…The presented data on complementreceptor subtypes are interesting in connection with our recent observations on the occurrence and distribution of complement receptor subtypes in follicular hyperplasia (Stein et al, 1978b). We found that EAC(3d usually adhered to germinal centres and the follicular mantle, whereas EAC3b adhered not only to germinal centres and the follicular mantle, but also to parafollicular areas and, in many instances, to interfollicular areas, but spared the T-dependent paracortical zone.…”

“…Those investigators showed that erythrocyte-antibody-complement complexes (EAC) prepared with whole mouse serum (EACmouse) as complement source adhered exclusively to germinal centres. Recently, our research group analysed the presence and distribution of D)r H. Steiin, Institute of Patliology, University of the complement-receptor subtypes (receptors for C3b and C3d) in reactive lymphoid tissue (Stein et al, 1978b). We found that GCC bear both complement-receptor subtypes.…”

Immuno-histological diagnosis of lymphoproliferative diseases by selected combinations of antisera and monoclonal antibodies

“…DURING RECENT YEARS non-Hodgkin lymphomas (NHL) have been characterized by immunological methods in a number of laboratories (Aisenberg & Long, 1975;Bloomfield et al, 1976;Braylan et al, 1975;Brouet et al, 1975;Lukes et al, 1978;Stein et al, 1978;Habeshaw et al, 1979). Staining of lymphocyte membrane antigens (with antisera) in formalin-fixed paraffin-embedded tissues has yielded variable results (Braylan & Rappaport, 1973;Taylor, 1978).…”

“…Thus most of the published studies have been carried out on suspensions of cells obtained from teased lymph nodes, a technique which is better suited to the requirements of membranemarker analysis. These studies have demonstrated that most lymphomas are of B-lymphoid origin and express "monoclonal" surface-membrane immunoglobulin (SmIg; with K or A light chain) and that complement receptors, Fc receptors and the capping characteristics of SmIg distinguish histologically distinct types of B lymphomas (Jaffe et al, 1974;Stein et al, 1978;Habeshaw et al, 1979). A small proportion of lymphomas have been shown to be of T-cell origin (Lukes & Collins, 1974;Bloomfield et al, 1976;Koziner et al, 1977;Stein et al, 1976;Waldron et al, 1977).…”

“…Other monoclonal antibodies reacting with T cells , T-cell subsets (Reinherz et al, , 1980, B cells and B cell subsets (Brooks et al, 1980) will further advance the immunological analysis of NHL, especially if used in appropriate combinations with other anitisera. The use of a panel of antibodies against B-cell subsets would be important, since the analysis of receptor profiles on these subsets already reveal remarkable (but not absolute) correlations with the histological pattern of NHL, and show prognostic significance (Habeshaw et al, 1979;Stein et al, 1978).…”