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Induction of Murine Intestinal Inflammation by Adoptive Transfer of Effector CD4+CD45RBhigh T Cells into Immunodeficient Mice
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Cd1d-restricted cellular lysis by peripheral blood lymphocytes: relevance to the inflammatory bowel diseases

M J Page1, L S Poritz, A F Tilberg

  • 1Department of Surgery, Pennsylvania State University College of Medicine, 500 University Drive, Hershey, Pennsylvania, 17033, USA. mpage@psghs.edu

The Journal of Surgical Research
|July 18, 2000
PubMed

Insights

CD1d molecule upregulation in inflammatory bowel diseases (IBD) suggests circulating immune cells may trigger intestinal inflammation and its related symptoms. This points to CD1d-specific antigen recognition in immune regulation.

Area of Science:

  • Immunology
  • Gastroenterology

Background:

  • The CD1d molecule is implicated in inflammatory bowel diseases (IBD).
  • Its role may involve presenting intestinal antigens that trigger immune responses.
  • Understanding CD1d's function in IBD is crucial for therapeutic development.

Purpose of the Study:

  • To investigate CD1d molecule expression in inflamed intestinal tissues from IBD patients.
  • To determine if lymphocytes from IBD patients recognize CD1d in a specific manner.
  • To elucidate the potential role of CD1d in the pathogenesis of IBD.

Main Methods:

  • Assessing CD1d expression in diseased intestinal tissue.
  • Evaluating CD1d-specific cytotoxicity by lymphocytes (intraepithelial and peripheral blood lymphocytes - PBLs) from IBD patients and controls.
  • Analyzing lymphocyte populations involved in CD1d recognition.

Main Results:

  • Increased precipitable CD1d was observed in inflamed tissues, indicating CD1d upregulation in IBD.
  • No CD1d-specific cytotoxicity was found by lymphocytes isolated from inflamed intestinal sites.
  • CD1d-specific cytotoxicity was mediated by PBLs from both IBD patients and normal controls, involving a unique lymphocytic cell type.

Conclusions:

  • Tissue-specific CD1d upregulation in IBD may initiate intestinal inflammation via circulating PBLs.
  • These activated PBLs could be responsible for extraintestinal manifestations associated with IBD.
  • The identified cells mediating CD1d-specific activity may regulate immune responses through CD1d-specific antigens.

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