Evidence for Two Shared Mechanisms Function: Directly Suppress CD3+/CD4+ Cell Pulmonary Surfactant Proteins A and D

SummaryWe have shown here that SP-A and SP-D from a variety of sourcesinhibited the proliferation of PBMC, plastic-nonadherent PBMC,and CD4 -depleted plastic-nonadherent cells that had been acti-vated with PMA and ionomycin. CD3 /CD4 cell proliferationwas also inhibited by SP-A or SP-D. The inhibition of phorbolester/calcium ionophore-induced proliferation of CD3 /CD4cells was not associated with a decrease in IL-2, IL-4, or IFN-secretion, nor could exogenous IL-2 rescue proliferation. SP-A andSP-D, but not C1q, inhibited the number of Th cells that pro-gressed into the G 2 M phase of the cell cycle. Conversely, wedemonstrated that these same preparations of SP-A and SP-D sup-pressed Ag-driven IL-2 production by OVA peptide-specific T cellhybridomas when splenocytes were used as a source of APC. Themechanism by which SP-A and SP-D suppress Th cell prolifera-tion was investigated by measuring one parameter important in thesignaling capacity of Th cells, [Ca ] . SP-A and SP-D bothreadily attenuated the release of large amounts of [Ca