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* Lymphocyte Biology Section, Division of Rheumatology, Immunology, and Allergy, Brigham and Women’s Hospital, Harvard Medical School, Boston, MA 02115;
Netherlands Cancer Institute, Antoni van Leeuwenhoek Hospital, Amsterdam, The Netherlands; and
Department of Environmental Health, Harvard School of Public Health, Boston, MA 02115
Upon exposure to Ag and inflammatory stimuli, dendritic cells (DCs)
undergo a series of dynamic cellular events, referred to as DC
maturation, that involve facilitated peptide Ag loading onto MHC class
II molecules and their subsequent transport to the cell surface.
Besides MHC molecules, human DCs prominently express molecules of the
CD1 family (CD1a, -b, -c, and -d) and mediate CD1-dependent
presentation of lipid and glycolipid Ags to T cells, but the impact of
DC maturation upon CD1 trafficking and Ag presentation is unknown.
Using monocyte-derived immature DCs and those stimulated with TNF-
for maturation, we observed that none of the CD1 isoforms underwent
changes in intracellular trafficking that mimicked MHC class II
molecules during DC maturation. In contrast to the striking increase in
surface expression of MHC class II on mature DCs, the surface
expression of CD1 molecules was either increased only slightly (for
CD1b and CD1c) or decreased (for CD1a). In addition, unlike MHC class
II, DC maturation-associated transport from lysosomes to the plasma
membrane was not readily detected for CD1b despite the fact that both
molecules were prominently expressed in the same MIIC lysosomal
compartments before maturation. Consistent with this, DCs efficiently
presented CD1b-restricted lipid Ags to specific T cells similarly in
immature and mature DCs. Thus, DC maturation-independent pathways for
lipid Ag presentation by CD1 may play a crucial role in host defense,
even before DCs are able to induce maximum activation of peptide
Ag-specific T cells.
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