Abstract
MOLECULES encoded by the human GDI locus on chromosome 1 (ref. 33) are recognized by selected CD4−8− T-cell clones expressing either αβ or γδ T-cell antigen receptors1,2. The known structural resemblance of GDI molecules to antigen-presenting molecules encoded by major histocompatibility complex (MHG) genes on human chromosome 6 (refs 3, 4, 34, 35), suggested that GDI may represent a family of antigen-presenting molecules separate from those encoded in the MHC1,5,6. Here we report that the proliferative and cytotoxic responses of human CD4−8− αβTCR+ T cells specific for Mycobacterium tuberculosis can be restricted by GDlb, one of the four identified protein products of the GDI locus. The responses of these T cells to M. tuberculosis seemed not to involve MHG encoded molecules, but were absolutely dependent on the expression of GDlb by the antigen-presenting cell and involved an antigen processing requirement similar to that seen in MHC class Il-restricted antigen presentation. These results provide, to our knowledge, the first direct evidence for the proposed antigen-presenting function of GDI molecules and suggest that the GDI family plays a role in cell-mediated immunity to microbial pathogens.
Similar content being viewed by others
References
Porcelli, S. et al. Nature 341, 447–450 (1989).
Faure, F., Jitsukawa, S., Miossec, C. & Hercend, T. Eur. J. Immun. 20, 703–706 (1990).
Calabi, F. & Milstein, C. Nature 323, 540–543 (1986).
Balk, S. P., Bleicher, P. A. & Terhorst, C. Proc. natn. Acad. Sci. U.S.A. 86, 252–256 (1989).
Strominger, J. L. Cell 57, 895–898 (1989).
Porcelli, S., Band, H. & Brenner, M. B. Immun. Rev. 120, 137–183 (1991).
Boumsell, L. in Leukocyte Typing IV (eds Knapp, W. et al.) 251–254 (1989).
Zenmour, J., Little, A.-M., Schendel, D. J. & Parham, P. J. Immun. 148, 1941–1948 (1992).
Balk, S. P. et al. Science 253, 1411–1415 (1991).
Salter, R. D., Howell, D. N. & Cresswell, P. Immunogenetics 21, 235–246 (1985).
Erlich, H., Lee, J. S., Petersen, J. W., Bugawan, T. & DeMars, R. Hum. Immun. 16, 205–219 (1986).
Parham, P. Nature 357, 193–194 (1992).
Hosken, N. A. & Bevan, M. J. Science 248, 367–370 (1990).
Wei, M. & Cresswell, P. Nature 356, 443–446 (1992).
Ziegler, H. K. & Unanue, E. R. Proc. natn. Acad. Sci. U.S.A. 79, 175–179 (1982).
Chesnut, R. W., Colon, S. M. & Grey, H. M. J. Immun. 129, 2382–2388 (1982).
Riberdy, J. M. & Cresswell, P. J. Immun. 148, 2586–2590 (1992).
Janeway, C. A. Jr, Jones, B. & Hayday, A. C. Immun. Today 6, 73–76 (1988).
Bluestone, J. A. & Matis, L. A. J. Immun. 142, 1785–1788 (1989).
Olive, D., Dubreuil, P. & Mawas, C. Immunogenetics 20, 253–264 (1984).
Glimcher, L. H. & Shevach, E. M. J. exp. Med. 156, 640–645 (1982).
Panchamoorthy, G. et al. J. Immun. 147, 3360–3369 (1991).
Reinherz, E., Kung, P. C., Goldstein, G., Levey, R. H. & Schlossman, S. F. Proc. natn. Acad. Sci. U.S.A. 77, 1588–1592 (1980).
Martin, L. H., Calabi, F., Lefebvre, F.-A., Bilsland, C. A. G. & Milstein, C. Proc. natn. Acad. Sci. U.S.A. 84, 9189–9193 (1987).
Brodsky, F. M. & Parham, P. P. J. Immun. 128, 129–135 (1982).
Lanier, L. L., Ruitenberg, J. J., Allison, J. P. & Weiss, A. in Leukocyte Typing III (ed. McMichael, A. J.) 175–178 (Oxford Univ. Press, Oxford, 1987).
Shiue, L., Gorman, S. D. & Parnes, J. R. J. exp. Med. 168, 1993–2005 (1988).
Anegon, I., Grolleau, D. & Soulillou, J. P. J. Immun. 147, 3973–3980 (1991).
Morita, C. T. et al. Eur. J. Immun. 21, 2999–3007 (1991).
Favaloro, E. J. et al. Disease Markers 4, 261–270 (1986).
Shaw, S., Ziegler, A. & DeMars, R. Hum. Immun. 12, 191–211 (1985).
Roncarolo, M. G. et al. J. Immun. 147, 781–787 (1991).
Albertson, D. G., Fishpool, R., Sherrington, P., Nacheva, E. & Milstein, C. EMBO J. 7, 2801–2805 (1988).
Martin, L. H., Calabi, F. & Milstein, C. Proc. natn. Acad. Sci. U.S.A. 83, 9154–9158 (1986).
Calabi, F., Jarvis, J. M., Martin, L. & Milstein, C. Eur. J. Immun. 19, 285–292 (1989).
Author information
Authors and Affiliations
Rights and permissions
About this article
Cite this article
Porcelli, S., Morita, C. & Brenner, M. CDlb restricts the response of human CD4−8−T lymphocytes to a microbial antigen. Nature 360, 593–597 (1992). https://doi.org/10.1038/360593a0
Received:
Accepted:
Issue Date:
DOI: https://doi.org/10.1038/360593a0
- Springer Nature Limited
This article is cited by
-
CD4 and CD8 co-receptors modulate functional avidity of CD1b-restricted T cells
Nature Communications (2022)
-
Clinically applicable CD34+-derived blood dendritic cell subsets exhibit key subset-specific features and potently boost anti-tumor T and NK cell responses
Cancer Immunology, Immunotherapy (2021)
-
A T-cell receptor escape channel allows broad T-cell response to CD1b and membrane phospholipids
Nature Communications (2019)
-
Conservation of molecular and cellular phenotypes of invariant NKT cells between humans and non-human primates
Immunogenetics (2019)
-
Molecular recognition of microbial lipid-based antigens by T cells
Cellular and Molecular Life Sciences (2018)