Abstract
Percutaneous exposure of C57Bl/6 strain mice to radiation-attenuated schistosome cercariae stimulates proliferation of Ag-specific T lymphocytes in the draining lymph nodes (LN), followed by an intense leukocytic infiltration into the pulmonary parenchyma and airways. The airway T cells persist at elevated levels at least up to 10 wk and will secrete IFN-gamma and IL-3 upon antigenic stimulation in vitro. We report here that more CD4+ T cells from the airways responded rapidly to mitogen by up-regulating the p55 subunit of the IL-2R than did splenocytes from the same animal, suggesting that the bulk of the pulmonary Th infiltrate comprised previously activated cells. A four-fold higher response to Ag indicated the greater abundance of schistosome-specific cells in the lungs than the spleen. Virtually all of the pulmonary CD4+ T cells expressed high levels of the memory marker CD44 (Pgp-1), in contrast with the situation in the draining LN and circulation where only a minority were in that category. Very few Th cells from the inflamed lung bound antibody to an epitope coded for by the B exon of CD45, unlike those from the LN and circulation; the antibody normally binds strongly to naive and weakly to memory CD4+ T cells. Overall, the airway CD4+ T lymphocytes in the schistosome-vaccinated mouse display the functional and phenotypic characteristics of short-term effector/memory cells. We believe that their presence endows the lung with the ability to respond rapidly to recall Ag in the form of challenge parasites.