Kinetics and characterization of antigen-binding and antibody-producing cells in the regional draining lymph nodes and spleen during initial murine schistosomiasis: I. Cellular responses against cercarial immunogens

Abstract

C57BL/6 mice were exposed to a primary infection of Schistosoma mansoni. The lymphocytes of the mediastinal, hepatic, and mesenteric lymph nodes and spleen which drain the pulmonary, hepatic, intestinal, and “systemic” phases of infection, respectively, were assessed for their ability to interact with soluble cercarial immunogen. The capacity to bind antigen, i.e., rosette-forming cells (B- or T-RFC) both bind antigen and simultaneously produce specific lytic antibodies, i.e., rosette-antibody-forming cells (RAFC); or exclusively produce specific antibody, i.e., plaque-forming cells (PFC) was assessed. The results indicated that maximal RFC were detected sequentially in the mediastinal (Week 1), then in the hepatic (Week 5), and finally in the mesenteric (Weeks 7–9) nodes; thus, the immune response anatomically recapitulated the migrating pathway of the parasite during the pulmonary, hepatic, and intestinal phases of the infection. The number of RFC was significantly higher in the mediastinal nodes and the hepatic nodes than in the mesenteric nodes. Although both T- and B-RFC were noted, the response was predominantly B in character. The spleen exhibited an early predominantly T-cell RFC response at Week 4 and a later predominantly B-cell RFC response at Week 11. Further characterization of the B-cell responses showed that the initial responses of the lymphocytes were predominantly IgM in nature. A variety of unique patterns relative to the predominance of IgG-, IgA-, or “IgE”-bearing cells subsequently evolved in each anatomic lymphoid organ. In all the lymphoid organs studied the lymphocytes exhibited a maturational progression from B-RFC, to RAFC and then to PFC. The responses of the lymphocytes of the various lymphoid organs have been further characterized against soluble egg (SEA) immunogen (P. B. Khoury and S. M. Phillips, Cell. Immunol. 59, 246, 1981).