摘要
共刺激分子CD40/CD40L及B7/CD28是T细胞活化的两条重要辅助刺激通路,不仅在调节T细胞免疫反应中起关键作用,而且也在B细胞的活化、增殖、分化、抗体的分泌起重要作用。近年来它们在动脉粥样硬化方面的研究成为国内外学者研究的热点。对共刺激分子和动脉粥样硬化关系的深入了解,将有助于阐明动脉粥样硬化发生的炎症和免疫机制,并为临床治疗开辟新途径。本文综述了共刺激分子的免疫学特征及功能以及在动脉粥样硬化中发挥的作用与免疫学治疗的前景。
Increasing evidence supports a central role for CD40/CD40L and B7/CD28 interactions in the pathogenesis of atherosclerosis. CD40/CD40L and B7/CD28 interactions play key roles in humoral and cellular immune responses. CD40, CD40L, B7 and CD28 protein are present in almost all cell types in human atherosclerosis, especially in advanced, rupture-prone and ruptured plaques. B7-1 （CD80） and B7-2 （CD86）, two members of B7 family, are members of the immunoglobulin superfamily, and they both bind to CD28 （ another Ig superfamily member） on resting T cells. CD40 and CD40L comprises Th-cell-driven activation, proliferation, and differentiation of B-lymphocytes, isotype switching primary T-lymphocyte response, and thymic selection. CD40L inhibition might be a novel therapeutic approach to prevent atherosclerotic plaque destabilization and plaque rupture. T-cell CD40L binding to CD40 on antigen-presenting cells enhances B7-1 and B7-2 expression, and B7-1/B7-2 co-stimulatory signals contribute to upregulation of CD40L. It will be important to characterize co-stimulatory molecule expression on plaque-antigen-presenting cells, and the interplay between B7 co-stimulatory and CD40/CD40L pathways within lesions. The possible expression of these molecules in plaques and their role in modulating atherosclerosis will be of great interest. This review discusses recent progress in understanding the role of CD40/CD40L and B7/CD28 molecules in atherosclerosis, and T-cell costimulation as an important link between innate immunity and adaptive immune responses.
出处
《国际内科学杂志》
CAS
2007年第8期467-470,共4页
International Journal of Internal Medicine
基金
广东省自然科学基金(项目编号0430054)
广东省科技计划项目:2006B36007003
