Alloreactivity and immunosuppressive properties of articular chondrocytes from osteoarthritic cartilage

被引:8
作者
Abe, Satomi [1 ]
Nochi, Hitoshi [1 ]
Ito, Hiroshi [1 ]
机构
[1] Asahikawa Med Univ, Dept Orthopaed Surg, Asahikawa, Hokkaido, Japan
关键词
chondrocytes; immune system; osteoarthritis; MESENCHYMAL STEM-CELLS; JOINT SURFACE-DEFECTS; ALLOGENEIC CHONDROCYTES; EPIPHYSEAL CHONDROCYTES; CLASS-II; RESPONSES; EXPRESSION; SURVIVAL; GROWTH; PROLIFERATION;
D O I
10.1177/1602400222
中图分类号
R826.8 [整形外科学]; R782.2 [口腔颌面部整形外科学]; R726.2 [小儿整形外科学]; R62 [整形外科学(修复外科学)];
学科分类号
摘要
Purpose. To determine whether articular chondrocytes derived from osteoarthritic knee joints could evoke alloreactive proliferation of peripheral blood mononuclear cells (PBMC) and inhibit mitogenic activity of polyclonally activated CD4(+) major histocompatibility complex (MHC) class II- restricted T cells in vitro. Methods. Osteoarthritic cartilages of 17 patients aged 61 to 85 years were harvested during total knee arthroplasty. Chondrocytes were cultured for experiments. PBMCs, CD4(+) T cells, CD8(+) T cells, and CD14(+) monocytes from healthy subjects were also used. To investigate the allogeneic response and immunosuppressive properties of chondrocytes, assays for one-way mixed lymphocyte reaction (MLR), apoptosis, activated CD4(+) T-cell proliferation, and cytotoxic CD8(+) T-cells were performed. Chondrocyte cell-surface antigens were examined using flow cytometry. Results. Chondrocytes failed to trigger an allogeneic PBMC reaction and did not include apoptosis of allogeneic PBMCs in the MLR assay. Chondrocytes inhibited the proliferation of polyclonally activated CD4(+) T cells via cell-cell contact and escaped the allogeneic cytotoxic reactivity of CD8(+) T cells. Chondrocytes expressed MHC class I but not MHC class II molecules or B7-1 / -2-positive co-stimulatory molecules. Conclusion. Chondrocytes from osteoarthritic knees in older patients exhibited similar immunomodulatory properties in vitro to those in juveniles or adults.
引用
收藏
页码:232 / 239
页数:8
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