ABSTRACT
Systhematized septal fibrosis of the liver can be induced in rats either by repeated intraperitoneal injections of pig-serum or by Capillaria hepatica infection. The relationship between these two etiological factors, as far as hepatic fibrosis is concerned, is not known, and present investigation attempts to investigate it. C. hepatica-induced septal fibrosis of the liver was considerably inhibited in rats previously rendered tolerant to pig-serum. Pig-serum-tolerant rats developed antibodies against pig-serum when infected with C. hepatica, but this did not happen when the infection occurred in normal rats. On the other hand, anti-C. hepatica antibodies failed to recognize any epitope in pig-serum, by Western blot. However, no evidence of an immunological cross reactivity was found, at least at the humoral level. Alternatively, cell-mediated mechanisms may be involved, and further investigations are warranted.
Subject(s)
Animals , Male , Female , Rats , Capillaria , Enoplida Infections , Liver Cirrhosis, Experimental , Liver Diseases, Parasitic , Antibodies, Helminth , Antigens, Helminth , Blotting, Western , Enzyme-Linked Immunosorbent Assay , Liver Cirrhosis, Experimental , Liver Diseases, Parasitic , Rats, Wistar , SwineABSTRACT
Immunological memory is embodied in the rapid and enhanced immune responsiveness to antigens that have been previously encountered. In this work we have analyzed the development of humoral immunological memory to a conventional antigen (TNP-BSA) and a superantigen (staphylococcal enterotoxin B (SEB) in T cell-reconstituted athymic or euthymic mice. It was demonstrated that T cell reconstituded athymic mice, which lack recent thymic emigrants, mount a primary response to a T cell dependent antigen, but do not develop memory or the capacity to produce specific anti-TNP IgG1 antibodies during the secondary immune response. On the other hand, if thymocytes were continously provided during the secondary response a typical memory response was achieved, with the presence of high levels of specific IgG1. In addition, we have shown that immunization of mice with staphylococcal enterotoxin B (SEB) resulted in a detectable anti-SEB antibody response, which was further increased upon boosting. The typical secondary response do SEB was mainly composed of IgG1, thus suggesting the involvement of interleukin-4 (IL-4)-producing T cells. These results led us to propose that the development of humoral immunological memory can not be solely explained by the long lifespan of primed T lymphocytes, and a novel dynamic and systemic hypothesis is given to explain memory development.