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Lymphocytes-b from the autoimmune-prone mouse strain mlr/1pr manifest an intrinsic defect in tetraparental mrl/1pr reversible dba/2 chimeras

Academic Article
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Overview

authors

  • Nemazee, David
  • Guiet, C.
  • Buerki, K.
  • Marshakrothstein, A.

publication date

  • October 1991

journal

  • Journal of Immunology  Journal

abstract

  • Data are presented showing that MRL/lpr in equilibrium DBA/2 tetraparental (allophenic) chimeras, unlike conventional lpr/lpr----+/lpr bone marrow chimeras, fail to develop graft-vs-host disease; instead they develop full-blown lymphoproliferation and autoantibody formation typical of unmanipulated MRL/lpr mice. The increase in the splenic and especially the lymph node mass is comprised predominantly of MRL/lpr-derived cells and all of the serum IgG2a is MRL/lpr derived. This dominance of MRL/lpr lymphoid activity occurred even in chimeras where greater than 90% of the skin and/or bone marrow cells were of the DBA/2 type. These results demonstrate the failure of the lpr environment to recruit normal B and T cells into the autoimmune process, the inability of normal cells to suppress MRL/lpr disease, and indicate further that the lpr mutation has an intrinsic effect on lymphocytes of both the B and T lineages.

subject areas

  • Animals
  • Arthritis
  • Autoimmunity
  • B-Lymphocytes
  • Chimera
  • Immune Tolerance
  • Immunoglobulin G
  • Lupus Erythematosus, Systemic
  • Mice
  • Mice, Inbred DBA
  • T-Lymphocytes
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Identity

International Standard Serial Number (ISSN)

  • 0022-1767

PubMed ID

  • 1918976
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Additional Document Info

start page

  • 2536

end page

  • 2539

volume

  • 147

issue

  • 8

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