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      Resident Corneal Cells Communicate with Neutrophils Leading to the Production of IP-10 during the Primary Inflammatory Response to HSV-1 Infection

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          Abstract

          In this study we show that murine and human neutrophils are capable of secreting IP-10 in response to communication from the HSV-1 infected cornea and that they do so in a time frame associated with the recruitment of CD8 + T cells and CXCR3-expressing cells. Cellular markers were used to establish that neutrophil influx corresponded in time to peak IP-10 production, and cellular depletion confirmed neutrophils to be a significant source of IP-10 during HSV-1 corneal infection in mice. A novel ex vivo model for human corneal tissue infection with HSV-1 was used to confirm that cells resident in the cornea are also capable of stimulating neutrophils to secrete IP-10. Our results support the hypothesis that neutrophils play a key role in T-cell recruitment and control of viral replication during HSV-1 corneal infection through the production of the T-cell recruiting chemokine IP-10.

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          Most cited references45

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          CD4+CD25+ T Cells Regulate Virus-specific Primary and Memory CD8+ T Cell Responses

          Naturally occurring CD4+CD25+ regulatory T cells appear important to prevent activation of autoreactive T cells. This article demonstrates that the magnitude of a CD8+ T cell–mediated immune response to an acute viral infection is also subject to control by CD4+CD25+ T regulatory cells (Treg). Accordingly, if natural Treg were depleted with specific anti-CD25 antibody before infection with HSV, the resultant CD8+ T cell response to the immunodominant peptide SSIEFARL was significantly enhanced. This was shown by several in vitro measures of CD8+ T cell reactivity and by assays that directly determine CD8+ T cell function, such as proliferation and cytotoxicity in vivo. The enhanced responsiveness in CD25-depleted animals was between three- and fourfold with the effect evident both in the acute and memory phases of the immune response. Surprisingly, HSV infection resulted in enhanced Treg function with such cells able to suppress CD8+ T cell responses to both viral and unrelated antigens. Our results are discussed both in term of how viral infection might temporarily diminish immunity to other infectious agents and their application to vaccines. Thus, controlling suppressor effects at the time of vaccination could result in more effective immunity.
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            Early events in HSV keratitis--setting the stage for a blinding disease.

            The last decade has seen herpes simplex virus (HSV)-induced stromal keratitis (SK) research shift from being a topic only of interest to vision researchers to one that fascinates the general field of inflammatory disease. Studies on experimental mouse lesions have uncovered several fundamental processes that explain lesion development. In this model, the chronic immuno-inflammatory lesions are mainly orchestrated by CD4+ T cells, but multiple early events occur that set the stage for the subsequent pathology. These include virus replication, the production of key cytokines and chemokines, neovascularization of the avascular cornea and the influx of certain inflammatory cell types. Many of these early events are subject to modulation, providing an approach to controlling this important cause of human blindness. We also comment on events ongoing during chronic SK, debating whether or not these represent virus-induced or autoimmune lesions.
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              Epidemiology of ocular herpes simplex. Incidence in Rochester, Minn, 1950 through 1982.

              Over the period 1950 through 1982, 122 Rochester, Minn residents had their first episode of ocular herpes simplex virus infection, for an age- and sex-adjusted incidence of 8.4 new cases per 100,000 person-years (95% confidence intervals [CI], 6.9 to 9.9 cases). These initial episodes involved lid or conjunctiva in 54%, superficial cornea in 63%, deeper cornea in 6%, and uveitis in 4%. An additional 29 residents had episodes of ocular herpes other than their first. Altogether, these 151 residents had 294 episodes of ocular herpes simplex infection, for an adjusted incidence of 20.7 episodes per 100,000 person-years (95% CI, 18.3 to 23.1 episodes). Age-adjusted rates by sex were comparable. There were no seasonal trends in incidence, but rates increased with time. On January 1, 1980, the prevalence of a history of ocular herpes simplex infection was 149 per 100,000 population (95% CI, 115 to 183).
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                Author and article information

                Journal
                Int J Inflam
                Int J Inflam
                IJI
                International Journal of Inflammation
                Hindawi Publishing Corporation
                2090-8040
                2042-0099
                2012
                15 March 2012
                : 2012
                : 810359
                Affiliations
                1Department of Biology, University of West Georgia, Carrollton, GA 30118, USA
                2Department of Microbiology and Immunology, University of South Alabama, Mobile, AL 36688, USA
                Author notes
                *S. J. Molesworth-Kenyon: smoleswo@ 123456westga.edu

                Academic Editor: Michelle C. Callegan

                Article
                10.1155/2012/810359
                3317199
                22518343
                7c8173c9-d711-4654-a29e-e7c649b407de
                Copyright © 2012 S. J. Molesworth-Kenyon et al.

                This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

                History
                : 12 October 2011
                : 28 November 2011
                : 19 December 2011
                Categories
                Research Article

                Immunology
                Immunology

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