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Articles in PresS, published online ahead of print September 13, 2002
Am J Physiol Lung Cell Mol Physiol, 10.1152/ajplung.00187.2002
Submitted on June 12, 2002
Accepted on September 4, 2002
1 Department of Cell Biology, Duke University Medical Center, Durham, NC, USA
* To whom correspondence should be addressed. E-mail: j.wright{at}cellbio.duke.edu.
Surfactant Protein A (SP-A) is an innate immune molecule that regulates pathogen clearance and lung inflammation. SP-A modulates innate immune functions such as phagocytosis, cytokine production, and chemotaxis; however, little is known about regulation of adaptive immunity by SP-A. Dendritic cells (DCs) are the most potent antigen-presenting cell with the unique capacity to activate naive T cells and initiate adaptive immunity. The goal of this study was to test the hypothesis that SP-A regulates the differentiation of immature DCs into potent T cell stimulators. The data show that incubation of immature DCs for 24 hours with SP-A inhibits basal- and LPS-mediated expression of MHC class II and CD86. Stimulation of immature DCs by SP-A also inhibits the allostimulation of T cells, enhances dextran endocytosis, and alters DC chemotaxis towards Rantes (CCR5) and SLC (CCR7). The effects on DC phenotype and function are similar for the structurally homologous C1q, but not for SP-D. These studies demonstrate that SP-A participates in the adaptive immune response by modulating important immune functions of DCs.
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