The Journal of Experimental Medicine
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Published online 17 July 2000.
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© The Rockefeller University Press, 0022-1007/2000/7/281/ $5.00
The Journal of Experimental Medicine, Volume 192, Number 2, July 17, 2000 281-288

Brief Definitive Reports

Human CD1b and CD1c Isoforms Survey Different Intracellular Compartments for the Presentation of Microbial Lipid Antigens

Volker Brikena, Robin M. Jackmanb, Gerald F.M. Wattsb, Rick A. Rogersc, and Steven A. Porcellia
a Department of Microbiology and Immunology, Albert Einstein College of Medicine, Bronx, New York 10461
b Division of Rheumatology, Immunology, and Allergy, Brigham and Women's Hospital, Harvard Medical School,Boston, Massachusetts 02115
c BioMedical Imaging Institute, Harvard School of Public Health, Boston, Massachusetts 02115

Correspondence to: Steven A. Porcelli, Department of Microbiology and Immunology, Albert Einstein College of Medicine, Rm. 416 Forchheimer Bldg., 1300 Morris Park Ave., Bronx, NY 10461. Tel:718-430-3228 Fax:718-430-8711 E-mail:porcelli{at}aecom.yu.edu.

CD1b and CD1c are antigen-presenting molecules that mediate recognition of bacterial lipids by T cells, but it is currently not known whether these two molecules are redundant or are specialized to perform different immunological functions. Here, we show that the distribution of CD1c in human dendritic cells was characterized by a high ratio of cell surface to intracellular molecules, whereas CD1b showed a reciprocal pattern of distribution. In contrast to the accumulation of CD1b in lysosomal major histocompatibility complex class II compartments, intracellular CD1c molecules accumulated in other endocytic compartments, most likely early and late endosomes. Deletion of the cytoplasmic tail of CD1c, containing a tyrosine-based internalization motif, abolished most of its intracellular localization. Functional studies using T cells specific for defined lipid antigens revealed that in contrast to CD1b-mediated antigen presentation, antigen presentation by CD1c was resistant to drugs inhibiting endosomal acidification and was independent of endosomal localization of CD1c. Taken together, these results support the hypothesis that CD1b and CD1c are specialized to survey the lipid content of different intracellular compartments.

Key Words: CD1, Mycobacterium tuberculosis, antigen presentation, intracellular trafficking, lipids


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