|
|
||||||||




* Division of Rheumatology, Immunology and Allergy,
Immunology Research Division, Department of Pathology, Brigham and Womens Hospital, Harvard Medical School, Boston, MA 02115;
Department of Microbiology and Immunology, Albert Einstein College of Medicine, Bronx, NY 10461; and
Center for Health Sciences, Division of Infectious Diseases, Department of Medicine, University of California Los Angeles School of Medicine, Los Angeles, CA 90095
Dendritic cells (DC) are potent APCs that sample Ags from the surrounding environment and present them to naive T cells using cell surface Ag-presenting molecules. The DC in both lymphoid and nonlymphoid tissues express high levels of CD1, a cell surface glycoprotein capable of presenting lipids and glycolipids to T cells. Distinct group 1 CD1 isoforms (CD1a, -b, -c) in man are known to traffic to different parts of the endocytic system where microbial Ags may be sampled. Guinea pigs are the only known rodent species that express the group 1 CD1 proteins. Therefore, we examined the expression and trafficking of guinea pig CD1 (gpCD1) isoforms on isolated DC. Confocal microscopy using mAbs specific for individual gpCD1 isoforms revealed differential trafficking of two distinct CD1b isoforms within DC. Colocalization of MHC class II was observed with the gpCD1b1 isoform, consistent with localization in the late endosomes of DC. In contrast, the gpCD1b3 isoform lacks an endosomal sorting motif and remains on the cell surface. Following incubation with Mycobacterium tuberculosis lipoarabinomannan, colocalization of endocytosed lipoarabinomannan with the gpCD1b1 isoform was observed but not with the gpCD1b3 isoform, which remained primarily on the cell surface. These data demonstrate that guinea pig DC express CD1 isoforms with unique trafficking patterns that recapitulate the patterns seen for human CD1 isoforms. This suggests evolutionary pressure for a conserved mechanism in mammals that allows CD1 to sample lipid Ags from various subcompartments of the endocytic system.
This article has been cited by other articles:
![]() |
I. Van Rhijn, D. C. Young, A. De Jong, J. Vazquez, T.-Y. Cheng, R. Talekar, D. C. Barral, L. Leon, M. B. Brenner, J. T. Katz, et al. CD1c bypasses lysosomes to present a lipopeptide antigen with 12 amino acids J. Exp. Med., June 8, 2009; 206(6): 1409 - 1422. [Abstract] [Full Text] [PDF] |
||||
![]() |
E. Carreras, S. Turner, V. Paharkova-Vatchkova, A. Mao, C. Dascher, and S. Kovats Estradiol Acts Directly on Bone Marrow Myeloid Progenitors to Differentially Regulate GM-CSF or Flt3 Ligand-Mediated Dendritic Cell Differentiation J. Immunol., January 15, 2008; 180(2): 727 - 738. [Abstract] [Full Text] [PDF] |
||||
![]() |
S. K. Dougan, A. Salas, P. Rava, A. Agyemang, A. Kaser, J. Morrison, A. Khurana, M. Kronenberg, C. Johnson, M. Exley, et al. Microsomal triglyceride transfer protein lipidation and control of CD1d on antigen-presenting cells J. Exp. Med., August 15, 2005; 202(4): 529 - 539. [Abstract] [Full Text] [PDF] |
||||
![]() |
Y. E. Latchman, S. C. Liang, Y. Wu, T. Chernova, R. A. Sobel, M. Klemm, V. K. Kuchroo, G. J. Freeman, and A. H. Sharpe PD-L1-deficient mice show that PD-L1 on T cells, antigen-presenting cells, and host tissues negatively regulates T cells PNAS, July 20, 2004; 101(29): 10691 - 10696. [Abstract] [Full Text] [PDF] |
||||
| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |