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Related Experiment Video

Updated: Jun 22, 2026

Induction of Murine Intestinal Inflammation by Adoptive Transfer of Effector CD4+CD45RBhigh T Cells into Immunodeficient Mice
08:37

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Published on: April 21, 2015

Blocking CD27-CD70 costimulatory pathway suppresses experimental colitis.

Monika Manocha1, Svend Rietdijk, Rietdijk Svend

  • 1Department of Pediatrics, Immune Disease Institute and Harvard Medical School, Boston, MA 02131, USA.

Journal of Immunology (Baltimore, Md. : 1950)
|June 16, 2009
PubMed
Summary

Blocking the CD70-CD27 interaction reduces T cell expansion and inflammation in experimental inflammatory bowel disease (IBD) models. This therapeutic approach may offer a potent treatment for IBD by targeting multiple pro-inflammatory cytokines.

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Area of Science:

  • Immunology
  • Gastroenterology
  • Cell Biology

Background:

  • Inflammatory bowel disease (IBD) pathogenesis involves CD4(+) T cell activation by antigen-presenting cells (APCs).
  • CD70, a costimulatory receptor, is expressed on specific APCs in the intestinal lamina propria.

Purpose of the Study:

  • To investigate the role of the CD70-CD27 interaction in experimental colitis development.
  • To evaluate the therapeutic potential of blocking this interaction in IBD models.

Main Methods:

  • Utilized two experimental IBD models in mice.
  • Employed adoptive transfer of naive CD4(+) T cells (CD27-deficient and wild-type).
  • Administered monoclonal anti-CD70 antibody (Ab) to assess disease prevention and amelioration.

Main Results:

  • CD27-deficient CD4(+) T cell transfer led to significantly less colitis.
  • Anti-CD70 Ab treatment prevented and ameliorated colitis induced by wild-type T cells.
  • Treatment reduced key pro-inflammatory cytokines: IL-6, TNF-alpha, and IFN-gamma.
  • Anti-CD70 Ab suppressed trinitrobenzene sulfonic acid-induced colitis.

Conclusions:

  • The CD70-CD27 interaction is critical for pathogenic T cell expansion in experimental colitis.
  • Blocking CD70-CD27 interaction with anti-CD70 Ab is a promising therapeutic strategy for IBD.
  • This approach may be more effective than targeting individual cytokines due to broad anti-inflammatory effects.