Site-restricted persistent cytomegalovirus infection after selective long-term depletion of CD4+ T lymphocytes.
TLDR
The CD8+ effector cells raised in the CD4 subset- deficient host were able of clear vital tissues from productive infection and to restrict asymptomatic, persistent infection to acinar glandular epithelial cells in salivary gland tissue.Abstract:
We have established a murine model system for exploring the ability of a CD4 subset-deficient host to cope with cytomegalovirus infection, and reported three findings. First, an antiviral response of the CD8 subset of T lymphocytes could be not only initiated but also maintained for a long period of time despite a continued absence of the CD4 subset, whereas the production of antiviral antibody proved strictly dependent upon help provided by the CD4 subset. Second, no function in the defense against infection could be ascribed as yet to CD4-CD8- T lymphocytes, which were seen to accumulate to a new subset as a result of depletion of the CD4 subset. This newly arising subset did not substitute for CD4+ T lymphocytes in providing help to B lymphocytes, and was also not effective in controlling the spread of virus in host tissues. As long as a function of these cells in the generation and maintenance of a CD8 subset-mediated response is not disproved, caution is indicated with concern to an autonomy of the CD8 subset. Third, even though with delay, the CD8+ effector cells raised in the CD4 subset-deficient host were able of clear vital tissues from productive infection and to restrict asymptomatic, persistent infection to acinar glandular epithelial cells in salivary gland tissue.read more
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ATF3 Protects against LPS-Induced Inflammation in Mice via Inhibiting HMGB1 Expression.
TL;DR: Upregulation of ATF3 contributes to the reduced release of inflammatory molecules, especially HMGB1, which induced lung injury and increased the survival rate of mice after LPS challenge, Therefore, suppressing LPS-induced inflammation with ATF3 induction or ATF3 mimetics may be an important strategy for sepsis therapy.
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The Influence of Interleukin 17A and IL17F Polymorphisms on Chronic Periodontitis Disease in Brazilian Patients
Joana Maira Valentini Zacarias,Emilia Sippert,Patrícia Yumeko Tsuneto,Jeane Eliete Laguila Visentainer,Cléverson O. Silva,Ana Maria Sell +5 more
TL;DR: In patients from Southern Brazil, the IL17A rs2275913 polymorphisms,IL17A AA genotype, and the A allele were associated with a susceptibility to chronic periodontitis.
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Trichomonas vaginalis Cysteine Proteinases: Iron Response in Gene Expression and Proteolytic Activity
Rossana Arroyo,Rosa Elena Cárdenas-Guerra,Elisa E. Figueroa-Angulo,Jonathan Puente-Rivera,Olga Zamudio-Prieto,Jaime Ortega-López +5 more
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Harnessing the Therapeutic Potential of Th17 Cells.
Jonas Bystrom,Taher E. Taher,M. Sherwan Muhyaddin,Felix I.L. Clanchy,Pamela Mangat,Ali S M Jawad,Richard O. Williams,Rizgar A. Mageed +7 more
TL;DR: A review of pathways through which Th17 subsets are induced, the molecular basis of their plasticity, and potential therapeutic strategies for their modulation in diseases is presented in this article.
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Andreas Habertheuer,Alfred Kocher,Günther Laufer,Martin Andreas,Wilson Y. Szeto,Peter Petzelbauer,Marek Ehrlich,Dominik Wiedemann +7 more
TL;DR: An increased understanding of the molecular players of ischemia reperfusion injury offers potential seeds for new cardioprotective regimens and may further displace boundaries of what is technically feasible.
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Therapy with monoclonal antibodies by elimination of T-cell subsets in vivo
TL;DR: It is shown here that unmodified monoclonal antibodies can be extremely effective at depleting cells in vivo and can be used for the selective manipulation of different aspects of the immune response.
Journal ArticleDOI
CD8-positive T lymphocytes specific for murine cytomegalovirus immediate-early antigens mediate protective immunity.
TL;DR: MCMV disease provides the first example of a role for nonstructural herpesvirus immediate-early antigens in protective immunity, and is shown to be mediated by virus-specific CD8+ CD4-T lymphocytes.
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