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Functional Characterization of Regulatory Macrophages That Inhibit Graft-reactive Immunity
Published on: June 7, 2017
Sequential analysis of HLA-C-specific killer cell inhibitory receptor (CD158b) expressing peripheral blood
1Department of Hematology and Oncology, Hokkaido University School of Medicine, Sapporo, Japan.
Insights
Natural killer cell receptors (KIRs) expression on CD158b-positive cells varied in patients with chronic graft-versus-host disease (cGVHD) after bone marrow transplant. Expanded CD158b-positive cells may help control alloresponse.
Area of Science:
- Immunology
- Transplantation immunology
Background:
- Allogeneic bone marrow transplantation (alloBMT) can lead to chronic graft-versus-host disease (cGVHD).
- Natural killer (NK) cell receptors, specifically KIRs for HLA-C (CD158b), play a role in immune regulation.
Observation:
- This study examined CD158b-positive cell expression in three cGVHD patients post-alloBMT.
- Patient 1: CD158b-positive cells increased with worsening cGVHD.
- Patient 2: High CD158b-positive cell levels correlated with cGVHD cure.
- Patient 3: Low CD158b-positive cell levels correlated with treatment non-response.
Findings:
- Chronic allostimulation appears to increase CD158b-positive cell populations.
- Expanded CD158b-positive cells may be associated with controlling allogeneic responses.
Implications:
- CD158b-positive cell levels could serve as a biomarker for cGVHD prognosis.
- Targeting or monitoring CD158b-positive cells might offer therapeutic strategies for cGVHD.
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.
