Elimination of both CD4+ and CD8+ T cells but not B cells eliminates inflammation and prolongs the survival of TGFβ1-deficient mice

Ramireddy Bommireddy, Sandra J. Engle, Ilona Ormsby, Gregory P. Boivin, George F. Babcock, Thomas Doetschman

Research output: Contribution to journalArticle

16 Scopus citations

Abstract

Transforming growth factor β1 (TGFβ1) is a potent negative immunoregulatory molecule. We have previously shown that the autoimmune-mediated weaning-age lethality of Tgfb1-/- mice is reversed upon genetic combination with Scid or Rag null alleles. Here, we show that elimination of T but not B cells is sufficient for the reversal, but elimination of either CD4+ or CD8+ cells is not. Although elimination of B cells does not rescue TGFβ1-deficient animals from autoimmunity, B cells are hyperresponsive to LPS in the absence of TGFβ1. TGFβ1 deficiency leads to activation of CD8+ T cells as suggested by down-modulation of CD8 even in the absence of CD4+ T cells. This study provides evidence that both CD4+ and CD8+ T cells, but not B cells, have the ability to cause inflammation in the absence of TGFβ1. However, though TGFβ1-deficient B cells are hyperresponsive to stimulation, alone they are not sufficient to cause inflammation.

Original languageEnglish (US)
Pages (from-to)96-104
Number of pages9
JournalCellular Immunology
Volume232
Issue number1-2
DOIs
StatePublished - Nov 1 2004
Externally publishedYes

Keywords

  • Cell proliferation
  • Growth factors
  • Inflammation
  • Knockout mice
  • T-lymphocytes and B-lymphocytes
  • TGFβ1

ASJC Scopus subject areas

  • Immunology

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