Location: Animal Disease ResearchTitle: Immunization-induced anaplasma marginale-specific T lymphocyte reponses impaired by A. marginale infection are restored after eliminating the infection with tetracycline Author
|Turse, Joshua - Washington State University|
|Deringer, James - Washington State University|
|Brown, Wnedy - Washington State University|
Submitted to: Clinical and Vaccine Immunology
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: 7/9/2014
Publication Date: 9/21/2014
Citation: Turse, J.E., Scoles, G.A., Deringer, J.R., Fry, L.M., Brown, W.C. 2014. Immunization-induced anaplasma marginale-specific T lymphocyte reponses impaired by A. marginale infection are restored after eliminating the infection with tetracycline . Clinical and Vaccine Immunology. 21(9):1369-75.
Interpretive Summary: Evasion of innate and adaptive immune responses occurs with many pathogenic bacteria that establish chronic infection. Anaplasma marginale is a tick-borne intraerythrocytic rickettsial pathogen of cattle that is found worldwide and causes anemia, reduced production and death in up to 30% of naive in cattle. Importantly, this pathogen is able to escape the bovine immune system and establish life-long persistent infection. Consequently development of a vaccine to prevent this disease is challenging. We are working toward understanding the bovine immune response to infection with A. marginale in order to help develop an effective vaccine. Our studies have shown that infection of A. marginale in cattle specifically suppresses the immune response directed against the pathogen and that bacterial infection is required to maintain the immune suppression. In order to be maximally effective, a vaccine will have to overcome this targeted immune suppression.
Technical Abstract: Infection of cattle with Anaplasma marginale fails to prime sustained effector/memory T-cell responses, and high bacterial load may induce antigen-specific CD4 T exhaustion and deletion. We tested the hypothesis that clearance of persistent infection restores the exhausted T-cell response. We show that infection-induced T-cell exhaustion, characterized as loss of antigen-specific proliferation, and gamma interferon (IFN-gamma) and tumor necrosis factor alpha (TNF-alpha) production are partially restored in cattle following clearance of persistent infection with tetracycline.