Wyckoff John H
Department of Veterinary Pathobiology, College of Veterinary Medicine, 250 McElroy Hall, Oklahoma State University, Stillwater, OK 74078-2007, USA.
Vet Microbiol. 2002 Dec 20;90(1-4):395-415. doi: 10.1016/s0378-1135(02)00224-9.
The long-held paradigm of T lymphocyte-mediated activation of mononuclear phagocytes (Mø) as the major mechanism of protection against facultative intracellular pathogens such as Brucella has been modified to include killing of infected Mø by various subsets of T lymphocytes. Remnants of killed infected cells are phagocytosed by immunologically-activated Mø, which are much more efficient at killing such pathogens. Most of the detailed information regarding immunity in general and that of brucellosis specifically has been obtained using murine infection models rather than in cattle. However, there has been considerable definition of cellular phenotypes, cytokines and functional characteristics of T lymphocytes in cattle over the last decade. This was mainly due to development of monoclonal antibodies against cell surface markers and application of molecular cloning and polymerase chain reaction (PCR) for isolation, characterization and detection of genes encoding bovine cytokines. This review discusses cellular and molecular immunity in bovine brucellosis as pertains to T lymphocyte interactions with the Mø. Although current knowledge directly obtained from brucellosis immunity studies in the bovine host is limited and incomplete, the many parallels between the bovine and murine immune systems allow for some extrapolation in the description of bovine host defense mechanisms. Direct information from studies with immunized cattle supports the concepts of coordinate activation of uninfected Mø and killing of Brucella-infected Mø by antigen-specific T lymphocytes as major mechanisms of host defense in bovine brucellosis. There also appears to be a bias in the T lymphocyte compartment towards recognition of particular bacterial stress proteins following immunization with live Brucella vaccines.
长期以来，T淋巴细胞介导单核吞噬细胞（Mø）活化被认为是抵御布鲁氏菌等兼性胞内病原体的主要保护机制，现在这一范式已有所改变，包括各种T淋巴细胞亚群对感染Mø的杀伤作用。被杀伤的感染细胞残余物被免疫激活的Mø吞噬，后者在杀灭此类病原体方面效率更高。关于一般免疫，特别是布鲁氏菌病免疫的大多数详细信息是通过小鼠感染模型而非牛获得的。然而，在过去十年中，牛的T淋巴细胞的细胞表型、细胞因子和功能特征已有相当明确的定义。这主要归功于针对细胞表面标志物的单克隆抗体的开发，以及分子克隆和聚合酶链反应（PCR）在牛细胞因子编码基因的分离、表征和检测中的应用。本综述讨论了牛布鲁氏菌病中的细胞免疫和分子免疫，涉及T淋巴细胞与Mø的相互作用。尽管目前直接从牛宿主布鲁氏菌病免疫研究中获得的知识有限且不完整，但牛和小鼠免疫系统之间的许多相似之处使得在描述牛宿主防御机制时可以进行一些推断。来自免疫牛研究的直接信息支持了以下概念：未感染的Mø协同激活以及抗原特异性T淋巴细胞杀灭布鲁氏菌感染的Mø是牛布鲁氏菌病宿主防御的主要机制。在用活布鲁氏菌疫苗免疫后，T淋巴细胞区室似乎也偏向于识别特定的细菌应激蛋白。
