Bovine T lymphocyte responses to Brucella abortus.


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.

Cite this paper

@article{Wyckoff2002BovineTL, title={Bovine T lymphocyte responses to Brucella abortus.}, author={John H Wyckoff}, journal={Veterinary microbiology}, year={2002}, volume={90 1-4}, pages={395-415} }