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<em>In vivo</em> modulation of thymus-derived lymphocytes with monoclonal antibodies in mice I. EFFECT OF ANTI-THY-1 ANTIBODY ON THE TISSUE DISTRIBUTION OF LYMPHOCYTES.

Authors :
Le Gros, G. S.
Prestidge, R. L.
Watson, J. D.
Source :
Immunology; Dec83, Vol. 50 Issue 4, p537-546, 10p
Publication Year :
1983

Abstract

A procedure is described for the in vivo removal of all detectable T lymphocytes from spleen and lymph nodes in mice. A single intraperitoneal injection of monoclonal anti-Thy-T antibody into mice leads to rapid depletion of functional I cells from peripheral lymphoid organs, but not thymus. The extent of T-celI depletion is dependent on the cytotoxic titre of the anti-Thy-I antibody used. Antibody with a median cytotoxic titre greater than 10&lt;superscript&gt;6&lt;/superscript&gt; causes the complete removal of cells bearing Thy-I, Lyt-I and Lyt-2 surface antigens from peripheral lymphoid populations in 3 days. Eight days after treatment Thy-I &lt;superscript&gt;+&lt;/superscript&gt;, Lyt-I &lt;superscript&gt;+&lt;/superscript&gt; and Lyt-2&lt;superscript&gt;+&lt;/superscript&gt; cells begin to reappear in these organs. Splenic B cells, assayed by the expression of surface immunoglobulin (sig) and by mitogenic responsiveness to bacterial lipopolysaccharide (LPS), are not affected by this treatment. The monoclonal anti-Thy-i antibody does not appear to penetrate thymus tissue and bind to thymocytes. Anti-Thy-I antibody, but not F(ab&#39;)&lt;subscript&gt;2&lt;/subscript&gt;, is required for in-vivo T-cell depletion. These findings indicate that anti-Thy-I antibody causes the removal of Thy-i &lt;superscript&gt;+&lt;/superscript&gt; cells from peripheral lymphoid tissue, and as the circulating levels of anti-Thy-I antibody decrease, cells from the thymus repopulate the thymus-dependent areas of the depleted lymphoid organs. [ABSTRACT FROM AUTHOR]

Details

Language :
English
ISSN :
00192805
Volume :
50
Issue :
4
Database :
Complementary Index
Journal :
Immunology
Publication Type :
Academic Journal
Accession number :
13399666