The leukocyte-common antigen (CD45) complex and B-lymphocyte activation.

In view of the changes reported in expression of the different members of the leukocyte-common family of antigens by T cells as they are activated, B cells were examined with monoclonal antibodies against p220-180 (CD45), p220,205 (CD45R), and p180 (UCHL1). Resting tonsil B cells reacted with CD45 and CD45R antibodies, but not with UCHL1. Activation of B cells by anti-IgM and IL-4 and culture of activated B cells with factors which induce proliferation (B-cell growth factor) and differentiation (IL-6) led to only minor changes in the expression of CD45, CD45R, and p180 antigens. Activation with phorbol ester led to minor increases in reactivity with CD45 and CD45R antibodies and led to a weak reactivity with UCHL1. The results suggest that the functional relationship previously described in T cells between p180 and p220,205 is not seen in B cells. p180 is induced, but only at low levels and only with nonphysiologic activation. CD45R is not lost under the same conditions. However, in terminally differentiated B cells, and in some chronic lymphocytic leukemias, p180 expression was seen, often coexpressed with CD45R.

The p24 leucocyte membrane antigen: modulation associated with lymphocyte activation and differentiation.

Monoclonal antibodies of the CD9 cluster recognize a 24 kD protein (p24) found on platelets and endothelium, and expressed by lymphocytes at restricted stages of maturation and activation. In this study, we explore the possibility that p24 is involved in the response of lymphocytes to signals delivered by lymphokines. p24 is expressed only very weakly by resting B lymphocytes. We found no increase in expression when cells were activated with anti-immunoglobulin together with interleukin-4, or induced to proliferate by low-molecular weight B cell growth factor (LMW-BCGF). Culture of activated B cells with B cell differentiation factor was associated with an increased mean expression of p24. In cells from a patient with chronic lymphocytic leukaemia (CLL), culture with LMW-BCGF up-regulated p24 expression. Resting T cells (p24-negative) were induced to express p24 strongly when activated with antibody against CD3. CD9 antibody did not modulate B or T cell responses to activation stimuli. The results suggest that the p24 molecule is not involved in the primary interaction of cells with lymphokine, but rather may be involved in a secondary reaction, such as ion flux, which follows as a consequence of the action of lymphokines on cells.

Further characterization of human myeloid antigens (gp160,95; gp150; gp67): investigation of epitopic heterogeneity and non-haemopoietic distribution using panels of monoclonal antibodies belonging to CD-11b, CD-13 and CD-33.

We have investigated the binding of over 30 different monoclonal antibodies (MAB) belonging to three distinct clusters of differentiation (CD-11b; CD-13; CD-33; as defined by the Third International Workshop on Leucocyte Differentiation Antigens (ILWS), 1986), and which are reactive with three distinct myeloid restricted surface antigens ('gp160,95'; 'gp150'; 'gp67'). By investigating reactivity with non-haemopoietic cells, we have confirmed that CD-11b and CD-33 MAB reactivity is largely restricted to haemopoietic cells, whilst CD-13 MAB showed additional binding to a wide range of non-haemopoietic cells. Epitopic heterogeneity was also investigated within each cluster of differentiation. Tested anti-CR3 (CD-11b) MAB varied in their ability to block the binding of complement coated sheep red blood cells and zymosan particles. A more detailed analysis of MAB binding heterogeneity was performed by competitive inhibition assays. It was demonstrated that MAB from both CD-11b and CD-13 bind to several distinct epitopes (at least six and five respectively) on their respective antigen molecules. In contrast, CD-33 MAB appear to bind to only a single site on 'gp67'. These data may allow for a clearer appreciation of the disparate functional effects obtained using different MAB reagents to individual myeloid antigens, as reported by a number of workers.