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Sequential analysis of HLA-C-specific killer cell inhibitory receptor (CD158b) expressing peripheral blood mononuclear cells during chronic graft-versus-host disease.

Abstract
We have sequentially investigated the expression of natural killer cell inhibitory receptors (KIRs) for HLA-C (CD158b) on peripheral blood mononuclear cells (PBMC) in three patients with extensive chronic graft-versus-host disease (cGVHD) after allogeneic bone marrow transplantation (alloBMT). Clinical symptoms of cGVHD were not cured and worsened in the first patient whose CD158b-positive cells increased to 18.5% during cGVHD and decreased to 9.4% at 8 months after transplantation. On the other hand, cGVHD was cured and did not relapse in the second patient whose CD158b-positive cells increased up to 45.9% during cGVHD and sustained 19.4% at 8 months after transplantation. In contrast, CD158b-positive cells were less than 10% during the course of cGVHD in the third patient, and her cGVHD did not respond to treatment. Therefore, it appears that chronic allostimulation augments the expansion of CD158b-positive cells and these expanded CD158b-positive cells may have some role in the control of alloresponse in some patients.
AuthorsJ Tanaka, Y Tutumi, A Mori, S Ohta, S Kobayashi, M Asaka, M Imamura
JournalBone marrow transplantation (Bone Marrow Transplant) Vol. 26 Issue 3 Pg. 287-90 (Aug 2000) ISSN: 0268-3369 [Print] England
PMID10967567 (Publication Type: Case Reports, Journal Article, Research Support, Non-U.S. Gov't)
Chemical References
  • Epitopes
  • HLA-C Antigens
  • Receptors, Immunologic
  • Receptors, KIR
  • Receptors, KIR2DL3
Topics
  • Adult
  • Bone Marrow Transplantation (immunology)
  • Chronic Disease
  • Epitopes (blood, immunology)
  • Female
  • Graft vs Host Disease (blood, immunology)
  • HLA-C Antigens (blood, immunology)
  • Humans
  • Killer Cells, Natural (immunology)
  • Leukocytes, Mononuclear (immunology, metabolism)
  • Male
  • Receptors, Immunologic (biosynthesis, blood, immunology)
  • Receptors, KIR
  • Receptors, KIR2DL3

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