Almost all IL-10+/CD4+ T cells were IL-4? (Physique 4b) and few were Foxp3+ (Physique 4c), a phenotype indicative of Tr1 cells. inflammatory disease, infertility, and risk of ectopic pregnancy, which can Cd163 be life-threatening. 3 Epidemiologic and clinical studies provide strong evidence that gonorrhea significantly increases the risk of acquisition and transmission of HIV. 1,4 typically triggers an intense inflammatory response characterized by an influx of neutrophils into the genital tract, yet natural gonococcal contamination does not induce a state of specific protective immunity. 5,6 Individuals with Methoxatin disodium salt gonorrhea are usually not guarded from reinfection, although one study reported partial protection against the same serovar of probably contributes to the continuing prevalence of this sexually transmitted contamination, and challenges the development of a vaccine against it. The conventional working hypothesis holds that can evade host immune defenses by multifactorial strategies including continuous changes in its surface antigenic structure, resistance to complement-mediated bacteriolysis, and possibly the production of IgA1 protease. 5,8C10 However, increasing evidence indicates that as a highly adapted pathogen has evolved specialized mechanisms to proactively suppress specific immune responses and promote growth and persistence in the host. For example, it has been exhibited that opacity (Opa) proteins are able to bind carcinoembryonic antigen-related cellular adhesion molecule (CEACAM)-1 on activated human CD4 T cells and down-regulate their activation and proliferation. 11 Recently, Zhu et al reported that could inhibit both human and mouse antigen-dependent CD4 T cell proliferation through interactions with host antigen presenting dendritic cells.12 Although it has been recognized that possesses the capacity to modulate host immune responses, the underlying mechanisms remain to be elucidated. Furthermore, comprehension of how this can be manipulated to Methoxatin disodium salt generate protective adaptive immunity against the organism is limited. Our previous studies in a mouse model of gonococcal contamination have exhibited that elicits Th17 responses which are involved in the influx of neutrophils to the genital tract as well as the recruitment of other innate defense mechanisms. 13 In contrast, can selectively suppress Th1 and Th2 activity of mouse CD4 T cells, and induction of TGF- plays a critical role in these differential effects. 14,15 Blockade of TGF- diverts Methoxatin disodium salt the pattern of host immune responses to and enhances specific protective immunity against the pathogen. However, we found that total inhibition of TGF- activity only partially reverses on Th1/Th2-mediated adaptive immune responses. IL-10 is usually a regulatory cytokine produced by a variety of immune cells including activated T cells, monocytes/macrophages, B cells, dendritic cells, and mast cells, 16 and it plays a major role in suppressing immune and inflammatory responses and maintaining specific T cell tolerance in both humans and mice. 17 Type 1 regulatory T (Tr1) cells are one type of induced regulatory T cells, which inhibits Th1, Th2, and Th17 immunity through the production of immunosuppressive cytokines, mainly IL-10. 18 Tr1 cells arise in the periphery when na?ve CD4+ T cells are activated by tolerogenic antigen-presenting cells in the presence of IL-10. 19 Therefore, the biological functions of IL-10 and Tr1 cells are closely related to each other. IL-10 is not only responsible for the regulatory effect of Tr1 cells but is also fundamental for their generation. Accumulating evidence indicates that IL-10 and Tr1 cells play a key role in regulating mucosal immune activation, for example, in the maintenance of gut immune homeostasis and tolerance to food antigens and enteric microbiota. 20,21 In addition, IL-10 and Tr1 cells are exploited by many pathogens at mucosal sites to evade protective immunity, including and and strongly induced the production of IL-10 and Tr1 cells, which are critically involved in the suppression of.
Almost all IL-10+/CD4+ T cells were IL-4? (Physique 4b) and few were Foxp3+ (Physique 4c), a phenotype indicative of Tr1 cells
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