Elsevier

Cellular Immunology

Volume 127, Issue 1, 15 April 1990, Pages 1-11
Cellular Immunology

Lymphocyte migration into brain modelled in vitro: Control by lymphocyte activation, cytokines, and antigen

https://doi.org/10.1016/0008-8749(90)90109-5Get rights and content

Abstract

Factors controlling lymphocyte adhesion to brain endothelium were investigated in vitro. Mitogen activation of lymphocytes causes increased adhesion to endothelium, which is maximal at 7–24 hr, declines to normal levels after the cells divide, and requires protein synthesis. Rat brain endothelium can be stimulated with IFN-γ to increase its adhesion to either normal or activated lymphocytes. The endothelium is sensitive to low levels of cytokine: adhesion develops rapidly after stimulation and requires new protein synthesis. Antigen-specific line cells also adhere more effectively to endothelium than normal lymph node cells. This is enhanced by IFN-γ treatment of the endothelium and is further increased marginally in the presence of the cognate antigen. The results suggest that either local stimulation of endothelium with cytokines or lymphocyte activation in the periphery will modulate lymphocyte traffic into brain.

References (21)

  • U. Traugott et al.

    Science

    (1983)
  • Y. Matsumoto et al.

    J. Immunol

    (1986)
  • C.C.W. Hughes et al.

    Immunology

    (1988)
  • T.B. Issekutz et al.

    Immunology

    (1986)
  • M.L. Dustin et al.

    J. Immunol

    (1986)
  • T. Springer et al.

    Annu. Rev. Immunol

    (1987)
  • T. Collins et al.

    J. Immunol

    (1984)
  • J.S. Pober et al.

    J. Immunol

    (1986)
  • D.E. Cavender et al.

    J. Immunol

    (1986)
  • C.C.W. Hughes et al.

    Neurosci. Lett

    (1986)
There are more references available in the full text version of this article.

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This work was supported by grants from the Medical Research Council of Great Britain and the Wellcome Trust.

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