A B S T R A C T Human lymphocytes from normal peripheral blood, thymus, spleen, thoracic duct, and peripheral lymphocytes from patients with chronic lymphatic leukemia were studied for complement receptor sites (CRL), surface immunoglobulin (SIg), and for the ability to form rosettes with sheep erythrocytes (TRFC). The two B cell markers (CRL and SIg) were found to be in overlapping, but not totally identical populations, whereas cells that were able to form rosettes were found in a totally unrelated population of lymphocytes; TRFC is therefore probably a reliable marker for T cells. In peripheral blood 24% of lymphocytes had SIg, but only half of these were also CRL. Almost all of the non-SIg peripheral blood lymphocytes were TRFC. In the spleen and thoracic duct only a few lymphocytes were observed that had SIg and were not CRL. On the other hand, in two of three spleens studied 10-20% of cells were CRL that did not have SIg. In the thoracic duct all non-CRL, non-SIg cells were TRFC. In chronic lymphatic leukemia three findings were made: (a) The presence or absence of CRL was independent of the presence or absence of SIg so that in individuals whose cells were non-SIg, CRL were usually plentiful.

According to the clonal selection theory, antigen selects out cells genetically precommitted to make antibody directed toward it, and stimulates them to produce antibody of that particular specificity. The simplest mechanism by which this selection might occur would be to postulate the presence of preformed antibody as the recognition unit. This prediction has stimulated several laboratories to investigate the presence of these recognition antibody molecules oll cell surfaces. The first indirect demonstration of immunoglobulin on the surface of lymphoid cells was the study of Sell and Gell (1) who used a variety of anti-immunoglobulin antisera to stimulate blast transformation of normal lymphoid cells. Subsequently, the capacity of a small portion of a lymphocyte population to react with specific antigen has been demonstrated by means of antigen-coated bead columns (2) and by the use of highly labeled radioactive antigen and radioautographic techniques (3, 4). Finally, recent studies using radioiodinated and fluorescein-conjugated anti-immunoglobulin antisera have shown the presence of detectable amounts of immunoglobulin on the surface of some small lymphocytes (5).The purpose of the present stud)" was to confirm and extend these latter observations by studying the distribution of the known classes of mouse immunoglobulins in the various lymphoid organs under different experimental conditions. Also, by use of a sensitive radioactive antigen-antibody assay system the amount of surface immunoglobulin present on the lymphoid cells was quantitated.* This is publication number 433 from

In the study of the role of lymphocytes in the immune response it is becoming increasingly apparent that lymphocyte membrane-bound receptors represent the recognition link between an antigen on the outside of the lymphocyte and the genetic capacity of the bTnphocyte to respond to stimulation. The first described antigen receptor was surface-bound immunoglobulin that characterizes bone marrow-derived lymphocytes (B cells) 1 and that is absent in any appreciable quantity from thymus-derived lymphocytes (T cells) (1-4). This surface-bound immunoglobulin is similar to humoral antibody and presumably/unctions as an antigen receptor with a high degree of specificity for individual antigens. B cells also have receptors for both the antibody (5, 6) and complement, C3, (7, 8) contained in immune complexes. The probable function of these latter two receptors is less clear and it was thought that since they require preformed antibody in order to react with antigen, they might function only in detection of antigens in the secondary immune response. Recently, however, it was shown that a complement receptor could bind fluid phase C3 (9) and other workers demonstrated that fluid phase C3 was apparently required for B cell activation in the primary immune response (10). The complement receptor may therefore play a key role in the primary immune response.