Advertisement

Kinetics of Rat Thymic Dendritic Cells in Bone Marrow-Reconstituted Radiation Chimeras

  • Adrian M. Duijvestijn
  • Malgorzata B. Murawska
  • Boelo Meedendorp
  • Flip A. Klatter
  • Jaap Kampinga
  • Paul Nieuwenhuis
Part of the Advances in Experimental Medicine and Biology book series (AEMB, volume 237)

Abstract

The thymus meets unique microenvironmental conditions essential for pre-T cell maturation and generation of the complete T cell repertoire. During intrathymic development thymocytes acquire qualities essential for adequate immune functioning of T cells, such as tolerance for self, antigen receptors, and restriction to class I or II MHC antigens. With respects to restriction of T helper cells to class II (Ia) antigens of the MHC, it is more or less generally accepted that class II positive cells in the thymus control this aspect in T cell ‘education’. Potential candidates for regulating restriction of T helper cells to class II molecules are thymic reticular epithelial cells and bone marrow-derived thymic dendritic cells (DC), both known to be Ia+. Attending the question which cell type indeed is controlling class II restriction in the thymus, one can study T helper cell restriction to Ia antigens in allogeneic or semi-allogeneic bone marrow-reconstituted radiation chimeras (BMRRC) or thymus-grafted animals. Results obtained from these studies are conflicting, suggesting on one hand, that class II restriction of T cells is dictated by thymic epithelial cells (1), or on the other hand, that DC (antigen presenting cells) in the thymus are involved in this (2,3). Of crucial importance in such restriction studies is to know at what experimental stage the thymus can be considered class II-chimeric with respects to epithelial cell versus DC, viz. how long does it take in BMRRC for the recipient thymic DC to be replaced by allogeneic or semi-allogeneic donor type DC?

Keywords

Dendritic Cell Thymic Epithelial Cell Peripheral Lymphoid Tissue Dendritic Cell Population Medullary Area 
These keywords were added by machine and not by the authors. This process is experimental and the keywords may be updated as the learning algorithm improves.

Preview

Unable to display preview. Download preview PDF.

Unable to display preview. Download preview PDF.

References

  1. 1.
    D. Lo and J. Sprent. Nature 319: 672 (1986).PubMedCrossRefGoogle Scholar
  2. 2.
    D.L. Longo and R.H. Schwartz. Nature 287: 44 (1980).PubMedCrossRefGoogle Scholar
  3. 3.
    D.L. Longo, A.M. Kruisbeek, M.L. Davis and L.A. Matis. Proc.Natl.Acad.Sci.USA 82: 5900 (1985).PubMedCrossRefGoogle Scholar
  4. 4.
    F.G.M. Kroese, A.S. Wubbena, D. Opstelten, G.J. Deenen, E.H. Schwander, L. de Leij, H. Vos, S. Poppema, J. Volberda and P. Nieuwenhuis. Eur.J.Immunol. 17: 921 (1987).PubMedCrossRefGoogle Scholar
  5. 5.
    N. van Rooijen, N. Kors and R. van Nieuwmegen. J.Histochem.Cytochem. 32: 677 (1984).PubMedCrossRefGoogle Scholar
  6. 6.
    A.M. Duijvestijn, R. Schutte, Y.G. Köhler, C. Korn and E.C.M. Hoefsmit. Cell Tissue Res. 231: 313 (1983).PubMedCrossRefGoogle Scholar
  7. 7.
    L. Nagelkerken, B. Schutte, R.J.M. Stet and P.J.C. van Breda Vriesman. Scand. J. Immunol. (in press).Google Scholar
  8. 8.
    A.N. Barclay and G. Mayrhofer. J.Exp.Med. 153: 1666 (1981).PubMedCrossRefGoogle Scholar
  9. 9.
    A.M. Duijvestijn and A.N. Barclay. J. Leukocyte Biol. 36: 561 (1984).PubMedGoogle Scholar
  10. 10.
    E.C.M. Hoefsmit, A.M. Duijvestijn and E.W.A. Kamperdijk. Immunobiology 161: 255 (1982).PubMedCrossRefGoogle Scholar

Copyright information

© Plenum Press, New York 1988

Authors and Affiliations

  • Adrian M. Duijvestijn
    • 1
  • Malgorzata B. Murawska
    • 1
  • Boelo Meedendorp
    • 1
  • Flip A. Klatter
    • 1
  • Jaap Kampinga
    • 1
  • Paul Nieuwenhuis
    • 1
  1. 1.Department of Histology, Medical FacultyUniversity of GroningenThe Netherlands

Personalised recommendations