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Anaplasma marginale infection with persistent high-load bacteremia induces a dysfunctional memory CD4+ T lymphocyte response but sustained high IgG titers.
Title | Anaplasma marginale infection with persistent high-load bacteremia induces a dysfunctional memory CD4+ T lymphocyte response but sustained high IgG titers. |
Publication Type | Journal Article |
Year of Publication | 2010 |
Authors | Han, S, Norimine, J, Brayton, KA, Palmer, GH, Scoles, GA, Brown, WC |
Journal | Clin Vaccine Immunol |
Volume | 17 |
Issue | 12 |
Pagination | 1881-90 |
Date Published | 2010 Dec |
ISSN | 1556-679X |
Keywords | Anaplasma marginale, Anaplasmosis, Animals, Antibodies, Bacterial, Bacteremia, Blood, Cattle, CD4-Positive T-Lymphocytes, Immunoglobulin G, Spleen, Time Factors |
Abstract | Control of blood-borne infections is dependent on antigen-specific effector and memory T cells and high-affinity IgG responses. In chronic infections characterized by a high antigen load, it has been shown that antigen-specific T and B cells are vulnerable to downregulation and apoptosis. Anaplasma marginale is a persistent infection of cattle characterized by acute and chronic high-load bacteremia. We previously showed that CD4(+) T cells primed by immunization with an A. marginale outer membrane protein were rapidly deleted following infection. Furthermore, peripheral blood T cell responses to bacteria were not observed after acute infection was controlled, suggesting dysfunctional T cell priming to other A. marginale antigens. The current study more closely investigated the kinetics of A. marginale-specific CD4(+) T cell responses primed during infection. Frequent sampling of peripheral blood and spleens revealed that antigen-specific CD4(+) T cell responses were first detected at 5 to 7 weeks, but the responses were sporadic and transient thereafter. A similar pattern was observed in animals sampled weekly for nearly 1 year. Paradoxically, by 2 weeks of infection, cattle had developed high titers of A. marginale-specific IgG, which remained high throughout persistent infection. This dysfunctional CD4(+) T cell response to infection is consistent with continual downregulation or deletion of newly primed effector T cells, similar to what was observed for immunization-induced T cells following A. marginale infection. The failure to establish a strong memory T cell response during A. marginale infection likely contributes to bacterial persistence. |
DOI | 10.1128/CVI.00257-10 |
Alternate Journal | Clin. Vaccine Immunol. |
PubMed ID | 20943884 |
PubMed Central ID | PMC3008194 |
Grant List | R01 AI053692-09 / AI / NIAID NIH HHS / United States R01-AI053692 / AI / NIAID NIH HHS / United States R01-AI44005 / AI / NIAID NIH HHS / United States R37 AI044005-14 / AI / NIAID NIH HHS / United States T32-AI07025-30 / AI / NIAID NIH HHS / United States |