B- and T-lymphocytes in ocular disease.
B- and T-lymphocytes in ocular disease.
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DOI：
10.1016/s0161-6420(84)34256-7
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发表时间：
1984-06
期刊：
影响因子：
13.7
通讯作者：
F. Jakobiec;J. Lefkowitch;D. Knowles
中科院分区：
文献类型：
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作者：
F. Jakobiec;J. Lefkowitch;D. Knowles
由于我们有能力研究这些不同疾病中浸润物的 B 淋巴细胞和 T 淋巴细胞组成，眼部炎症性疾病和眼附属器淋巴肿瘤已变得不再那么模糊和令人生畏。还可以比较外周血中的淋巴细胞分布和眼组织本身内原位浸润物的精确组成。单克隆抗体的出现可以确定 T 淋巴细胞亚群，如 T 辅助细胞和 T 抑制/细胞毒性细胞、自然杀伤细胞和单核细胞-组织细胞，为描述炎症浸润的独特免疫成分以及 T 细胞免疫调节中任何可能的干扰提供了强大的技术。 B 淋巴细胞产生免疫球蛋白，在局部或全身性自身免疫性疾病中，免疫球蛋白可能被误认为是自身抗体。免疫球蛋白介导且因此由 B 细胞衍生的病症包括血管炎、进行性瘢痕性眼部类天疱疮、蚕蚀性角膜溃疡、巩膜炎、花粉热和春季结膜炎。 B淋巴细胞、其免疫球蛋白产物或与目前未知的抗原形成的免疫复合物可能导致的其他疾病是慢性非特异性葡萄膜炎；白塞氏综合征中的虹膜睫状体炎； Fuch异色综合征、强直性脊柱炎和Reiter综合征；格雷夫斯病；以及特发性炎性眼眶假瘤和肌炎。 T细胞不产生免疫球蛋白，而是分泌淋巴因子或直接与病毒或靶组织上的受体或决定簇相互作用（例如针对肿瘤的免疫监视）；一些自身免疫性疾病可能是宿主组织表面新抗原的结果，这些新抗原是由隐秘的刺激病毒编码的。 T细胞疾病包括静脉移植排斥反应、移植物抗宿主病以及可能的交感性眼炎和颞动脉炎。自然杀伤细胞与细胞毒性 T 细胞涉及许多相同的疾病，只是前者不需要致敏期（自然免疫），而细胞毒性 T 细胞必须经历抗原特异性母细胞转化（迟发型超敏反应类型的获得性免疫）。在许多 B 细胞衍生的自身抗体出现故障的疾病中，可能存在局部组织或全身 T 细胞失衡，T 抑制细胞减少，T 辅助细胞相对增多，从而促进错误定向的自身抗体的产生。在假性淋巴瘤中，病变处发现 T 细胞失衡；绝大多数附件淋巴是单克隆 B 细胞增殖。
Ocular inflammatory diseases and ocular adnexal lymphoid tumors have become less obscure and intimidating by virtue of our ability to study the infiltrates in these various diseases for their B-lymphocyte and T-lymphocyte composition. Comparisons are also possible between lymphocytic profiles in the peripheral blood and the precise composition of the in situ infiltrates within the ocular tissue themselves. The availability of monoclonal antibodies, which can determine T-lymphocytic subsets such as T-helper cells and T-suppressor/cytotoxic cells, natural killer cells, and monocytes-histiocytes, has provided a powerful technology for the delineation of the distinctive immune composition of the inflammatory infiltrates, as well as any possible disturbances in T-cell immunoregulation. B-lymphocytes produce immunoglobulins, which may be misdirected as autoantibodies in local or systemic autoimmune diseases. Immunoglobulin-mediated and therefore B-cell derived conditions include vasculitis, progressive cicatricial ocular pemphigoid, Mooren's corneal ulcer, scleritis, and hay fever and vernal conjunctivitis. Other diseases in which B-lymphocytes, their immunoglobulin products or immune complexes formed with presently unknown antigens are potentially at fault are chronic non-specific uveitis; iridocyclitis in Behcet's syndrome; Fuch's heterochromic syndrome, ankylosing spondylitis, and Reiter's syndrome; Graves' disease; and idiopathic inflammatory orbital pseudotumor and myositis. T-cells do not produce immunoglobins, but rather secrete lymphokines or interact directly with receptors or determinants on viruses or target tissues (eg. immunosurveillance against neoplasia); it is possible that some autoimmune diseases are the result of neo-antigens on the surfaces of host tissues that have been coded for by a cryptic inciting virus. T-cell diseases include phlyctenulosis graft rejections, graft versus host disease, and possibly sympathetic ophthalmia and temporal arteritis. Natural killer cells are involved in many of the same diseases as cytotoxic T-cells, except that the former require no period of sensitization (natural immunity), whereas cytotoxic T-cells must undergo an antigen-specific blast transformation (acquired immunity of the delayed hypersensitivity type). In many diseases in which B-cell derived auto-antibodies are at fault, there may be local tissue or systemic T-cell imbalances, with a reduction in T-suppressor cells and a relative augmentation in T-helper cells, thereby facilitating production of misdirected auto-antibodies. In pseudolymophomas, a T-cell imbalance has been discovered in the lesions; the vast majority of adnexal lympho are monoclonal B-cell proliferations.