The Forgotten Lymphocyte

Abstract

Inflammation is recognized as a key player in the development of atherosclerosis and is increasingly believed to contribute to reperfusion injury and delayed ischemia in the brain after stroke. The immune system is overwhelmingly complex; clinical interest in stroke and vascular disease has focused particularly on the roles played by specific immune cells and cytokines. Monocyte-macrophages and lymphocytes are the major immune cells within atherosclerotic lesions.1 Neutrophils and monocyte-macrophages are believed to exacerbate stroke-related ischemia-reperfusion injury.2 However, lymphocytes are key and versatile regulators of the immune system; their role during ischemic stroke may have been underappreciated. Evidence is now beginning to emerge that lymphocytes may have a greater and earlier involvement during stroke, opening the door for novel and highly specific targets for diagnostic, management, treatment, and prevention strategies for both stroke and vascular disease. Article p 2105 When the immune system becomes activated, a delicate balance between inflammatory and antiinflammatory states is maintained by the innate (nonspecific) and adaptive immune systems. The adaptive immune system is characterized by its ability to alter receptor expression and cellular functions when encountering new antigens, whether self or foreign; functions include cell-mediated immunity, humoral immunity, immune response regulation, memory, and immunological tolerance. Cells of the adaptive immune system include T-cell lymphocytes (helper T cells [generally CD4+] and cytotoxic T cells [generally CD8+]), natural killer cells, and B-cell lymphocytes. After antigenic activation, CD4+ T cells can be differentiated into at least 3 subsets: Th1 (which are involved in cell-mediated immunity and secrete proinflammatory cytokines such as gamma-interferon [γ-IFN], interleukin [IL]-2, and lymphotoxin), Th2 (which …