Chlamydia infections constitute a major public health problem. Although multiple arms of the immune system participate in the control of Chlamydia in infected hosts, T lymphocytes are essential. This review focuses on the roles that CD8 + T cells may play in immunoprotection and immunopathology following recognition of Chlamydia-infected cells. KeywordsChlamydia; CD8 + T cells IntroductionMembers of the Chlamydiaceae family are obligate intracellular gram-negative bacteria that include the human pathogens Chlamydia trachomatis (Ct) and Chlamydia pneumoniae (Cpn). While Ct is responsible for ocular and sexually transmitted diseases that can result in blindness and infertility, Cpn is a common cause of upper respiratory infections and pneumonia and has been associated with several chronic inflammatory conditions such as atherosclerosis and chronic obstructive pulmonary disease (COPD) [1][2][3]. When diagnosed early, Chlamydia infections can be treated with antibiotics. However, the high costs required to identify and treat individuals with mild or no symptoms limits the feasibility of this control strategy. Moreover, hosts can remain chronically infected despite chemotherapy, and some antibiotics may induce chlamydial persistence [4]. Thus, development of safe and effective vaccines represents a cost-effective approach that would have a greater impact on the high prevalence of Chlamydia infections and the prevention of severe long-term sequelae.Like all chlamydiae, Ct and Cpn have a unique biphasic developmental cycle alternating between an infectious metabolically inert elementary body (EB) and a replicating metabolically active reticulate body (RB). After entry into susceptible cells such as epithelial cells, macrophages, endothelial and smooth muscle cells, the EB remains within a nonacidified vacuole known as an inclusion, where it differentiates into a RB, which replicates by binary fission. The generated progeny differentiate back into EBs that are then released upon host cell lysis to infect other cells. Under certain conditions, however, Chlamydia enters a persistent non-replicating stage but remains capable of resuming a productive cycle when the adverse *Corresponding author. Current mailing address: Intercell AG, Campus Vienna Biocenter 6, 1030 Wien, Austria. Phone: +43-1-20620-174. Fax: +43-1-20620-805. E-mail: bwizel@intercell.com. Publisher's Disclaimer: This is a PDF file of an unedited manuscript that has been accepted for publication. As a service to our customers we are providing this early version of the manuscript. The manuscript will undergo copyediting, typesetting, and review of the resulting proof before it is published in its final citable form. Please note that during the production process errors may be discovered which could affect the content, and all legal disclaimers that apply to the journal pertain. NIH Public Access Evidence of a role for CD8 + T cells in the immune control of ChlamydiaAn intact T cell compartment is required for resistance against Chlamydia infection. T ...

The present study was carried out to test the immunostimulatory and adjuvant effects of the non‐toxic B subunit of cholera toxin (CTB), CpG oligodeoxynucleotide (ODN) and CpG ODN linked to CTB (CTB–CpG) for generation of immunity against H. pylori in mice. Herein, we showed that CTB–CpG induces more potent proinflammatory cytokine and chemokine responses in the cervical and the mesenteric lymph nodes (CLN and MLN, respectively) cells in vitro compared with those of CTB and CpG ODN. The adjuvant effects of these agents were examined following intranasal immunization of C57Bl/6 mice with H. pylori lysate in combination with CpG ODN, CTB or CTB–CpG. All three immunization regimes resulted in high H. pylori‐specific IgG antibody responses; however, only the CTB–CpG and, to some extent, the CpG ODN immunized mice mounted a sustainable IgG2c antibody response. Importantly, mice immunized with H. pylori antigen and CTB–CpG or CpG ODN, but not CTB, developed strong H. pylori‐specific proliferative and IFN‐γ responses in their MLN CD4+ T cells upon recall antigen stimulation in vitro. These mice also had significantly lower bacterial load compared with the control‐infected mice. Furthermore, the CTB–CpG and the CpG ODN immunized mice developed increased specific IgA antibody responses in their gastrointestinal tracts following H. pylori challenge. These results imply that CTB–CpG and CpG ODN, but not CTB, could serve as nasal adjuvants for induction of a H. pylori‐specific Th1 type immunity in MLN and also a specific mucosal IgA antibody response in the gastrointestinal tract upon H. pylori challenge.