Division of Rheumatology and Connective Tissue Research, Department of Medicine, University of Medicine and Dentistry of New Jersey-Robert Wood Johnson Medical School, New Brunswick, NJ 08903, USA.
J Clin Rheumatol. 2012 Mar;18(2):83-8. doi: 10.1097/RHU.0b013e318247bc64.
The full story of what surface markers mean about the cells on which they reside twists and turns as the days go by, with previously accepted "truth" changing in light of new findings. Such is the case with CD5, a surface marker on most murine T cells, many thymocytes, and a subset of B cells. The precise role of CD5 in the murine and human immune responses has been a matter of intense speculation for many years. Recent work suggests that CD5 may have a fine-tuning or suppressive effect on signaling through the antigen receptors on both B and T cells. These CD5 B cells were initially thought to be a major source of autoantibodies and/or "natural antibodies," targeting broad arrays of carbohydrate and protein antigens. More recent studies support the latter contention-CD5 B cells do produce "natural antibodies," but the former is far from true-CD5 B cells are not the major source of autoantibodies. In fact, CD5 may be a major negative influence on antigen receptor driven-B-cell function and may serve to control autoimmunity rather than encourage it. Furthermore, another subset of CD5 B cells may represent a distinct regulatory population. CD5 expression is noted on more than three fourths of all T-cell lymphomas. CD5 may be a receptor of pathogen-associated molecular patterns; CD5 may be a marker of decreased dependence of B cells on certain circulating factors. Elevated levels of CD5 are found in a number of autoimmune disorders. Thus, although the precise mechanism is unclear, there is at the very least circumstantial evidence of a role for CD5 in the pathogenesis of autoimmunity and perhaps T cell-derived lymphoid malignancy. New findings put old claims to rest and open up new avenues for research, both basic and clinical, with therapeutic applications not far behind.
随着时间的推移，关于表面标志物在其所在细胞上的意义的完整故事变得错综复杂，先前被接受的“真理”在新发现的影响下发生了变化。这种情况发生在 CD5 上，它是大多数鼠类 T 细胞、许多胸腺细胞和一部分 B 细胞上的表面标志物。CD5 在鼠类和人类免疫反应中的精确作用多年来一直是激烈猜测的问题。最近的工作表明，CD5 可能对 B 和 T 细胞上的抗原受体信号具有微调或抑制作用。这些最初被认为是产生自身抗体和/或“天然抗体”的主要来源的 CD5 B 细胞，针对广泛的碳水化合物和蛋白质抗原。最近的研究支持后一种观点——CD5 B 细胞确实产生“天然抗体”，但前一种观点远非事实——CD5 B 细胞不是自身抗体的主要来源。事实上，CD5 可能对抗原受体驱动的 B 细胞功能产生重大负面影响，并可能有助于控制自身免疫，而不是鼓励它。此外，CD5 B 细胞的另一个亚群可能代表一个独特的调节群体。超过四分之三的 T 细胞淋巴瘤都表达 CD5。CD5 可能是病原体相关分子模式的受体；CD5 可能是 B 细胞对某些循环因子的依赖性降低的标志物。在许多自身免疫性疾病中发现 CD5 水平升高。因此，尽管确切的机制尚不清楚，但至少有间接证据表明 CD5 在自身免疫和可能的 T 细胞衍生的淋巴恶性肿瘤的发病机制中发挥作用。新发现使旧的主张得到了平息，并为基础和临床研究开辟了新的途径，治疗应用也紧随其后。
