Russell John H
Program in Immunology, Department of Molecular Biology and Pharmacology, Washington University School of Medicine, St. Louis, MO 63110, USA.
Immunol Res. 2005;32(1-3):225-9. doi: 10.1385/IR:32:1-3:225.
Much of the understanding of tolerance has focused on the requirements for antigen-specific lymphocyte activation and function. However, there is increasing evidence for anatomic regulation of effector access to self antigens. Recently, a number of studies have provided evidence for tissue-specific "addressins" in chemokine/chemokine receptor pairs. The central nervous system (CNS) provides special anatomic barriers to the movement of cells from the vascular compartment to the parenchyma. Herein I raise the possibility that antigen, perhaps through specialized antigen-presenting cells, may play a role in regulating access of activated lymphocytes into the CNS parenchyma. The results suggest that a reexamination of the widely held dogma that all activated lymphocytes have access to the CNS parenchyma is necessary to understand the relationship between the immune and central nervous systems.
对免疫耐受的理解大多集中在抗原特异性淋巴细胞激活和功能的要求上。然而,越来越多的证据表明,效应细胞接触自身抗原存在解剖学调控。最近,多项研究为趋化因子/趋化因子受体对中的组织特异性“地址素”提供了证据。中枢神经系统(CNS)对细胞从血管腔室向实质移动提供了特殊的解剖学屏障。在此,我提出一种可能性,即抗原或许通过特殊的抗原呈递细胞,可能在调节活化淋巴细胞进入CNS实质的过程中发挥作用。这些结果表明,重新审视普遍认为所有活化淋巴细胞都能进入CNS实质这一教条,对于理解免疫系统与中枢神经系统之间的关系是必要的。