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Olive, A

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Olive, A
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    Immunity to Chlamydia trachomatis and Host-Pathogen Interactions During Infection
    (2014-02-25) Olive, A; Starnbach, Michael N.; Rubin, Eric; Galan, Jorge; Hacohen, Nir; Winau, Florian
    Infections with the bacterial pathogen Chlamydia trachomatis are a critical public health problem. Chlamydia remains the number one cause of preventable blindness worldwide and the leading cause of bacterial sexually transmitted infections in the United States. In humans, repeat and persistent infections with Chlamydia result in severe inflammation. Inflammation in the conjunctiva can result in blindness, while inflammation in the genital tract can result in pelvic inflammatory disease, ectopic pregnancy or infertility. In order to curb the increasing incidence of Chlamydia infections worldwide it will be necessary to develop a protective vaccine that affords long-term protection and prevents pathologies. To better inform vaccine development we must understand the mechanisms that drive long-term immunity in the genital tract and elucidate critical interactions between Chlamydia and host cells to uncover potential mechanisms of immune evasion.
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    A mucosal vaccine against Chlamydia trachomatis generates two waves of protective memory T cells
    (American Association for the Advancement of Science (AAAS), 2015) Stary, Georg; Olive, A; Radovic-Moreno, A. F.; Gondek, D.; Alvarez, David; Basto, P. A.; Perro, M.; Vrbanac, Vladimir; Tager, Andrew Martin; Shi, Jinjun; Yethon, J. A.; Farokhzad, Omid; Langer, Robert; Starnbach, Michael; von Andrian-Werburg, Ulrich
    Genital Chlamydia trachomatis (Ct) infection induces protective immunity that depends on interferon-γ producing CD4 T-cells. By contrast, mucosal exposure to ultraviolet light (UV)-inactivated Ct (UV-Ct) generated regulatory T-cells that exacerbated subsequent Ct infection. We show that mucosal immunization with UV-Ct complexed with charge-switching synthetic adjuvant particles (cSAP) elicited long-lived protection in conventional and humanized mice. UV-Ct-cSAP targeted immunogenic uterine CD11b+CD103− dendritic cells (DCs), whereas UV-Ct accumulated in tolerogenic CD11b−CD103+ DCs. Regardless of vaccination route, UV-Ct-cSAP induced systemic memory T-cells, but only mucosal vaccination induced effector T-cells that rapidly seeded uterine mucosa with resident memory T-cells (TRM). Optimal Ct clearance required both TRM seeding and subsequent infection-induced recruitment of circulating memory T-cells. Thus, UV-Ct-cSAP vaccination generated two synergistic memory T-cell subsets with distinct migratory properties.