Immunological effect of CB-11mAb on intervertebral disc degeneration

II型胶原存在于椎间盘的透明软骨和髓核中，作为免疫反应的分离抗原具有特异性。在考虑椎间盘退变的机制时，环破裂可能与体内髓核中的II型胶原蛋白和淋巴细胞有接触。在人类中，许多患者表现出严重的多发性椎间盘退变，而与他们的克隆年龄无关，这表明椎间盘退变具有免疫学背景。从透明软骨观察的实验结果来看，II型胶原的CB-11肽是Tⅱc免疫反应性的特异性片段。本课题对CB-11肽的特异性单克隆抗体（CB-11mAb）进行了大量的研究。前期研究从CB-11mAb对小鼠胶原性关节炎的免疫抑制结果中明确了CB-11mAb识别TⅱC抗原表位。采用ABC法，将手术获得的12个新鲜椎间盘（主要是不同程度退变的髓核）的连续免疫组化切片与CB-11mAb反应。然而，在退行性髓核中未观察到II型胶原的阳性免疫反应性。因此，在人类椎间盘退变过程中，t2c的免疫机制可以忽略不计。

Type II collagen existing in the hyaline cartilage and nucleus pulposus of the intervertebral disc have a specific property as an isolated antigen for immunological reactions.In considering the mechanism of intervertebral disc degeneration, annular rupture may provide contact with Type II collagen in the nucleus pulposus and the lymphocytes in vivo. In humans, not a few patients show severe multiple intervertebral disc degeneration irrespective of their clonological ages, suggesting an immulogical background to represent disc degeneration. From the experimental results of hyaline cartilage observation, CB-11 peptide of Type II collagen is a specific fragment of immunoreactivity of T II C.In this reserch project, mamy efforts have been paid to refine the specific monoclonal antibody of CB-11 peptide (CB-11mAb). The pilot study clarified that the CB-11mAb recognized the antigen epitope of T II C from the results of immunosuppressive efects of CB-11mAb on collagen-induced arthritis in mice. Using an ABC method, serial immunohistochemical sections from 12 fresh intervertebral discs (mainly nucleus pulposus with various grade of degeneration) obtained by surgery was reacted with the CB-11mAb. However, none of positive immunoreactivity of Type II collagen was observed in degenerated nucleus pulposus.Thus the conclusion was drawn to be negligible on T II C immunologic mechanism on the process of intervertebral disc degeneration in humans.