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  • The American Association of Immunologists  (5)
  • Medicine  (5)
  • 1
    Online Resource
    Online Resource
    The American Association of Immunologists ; 2000
    In:  The Journal of Immunology Vol. 164, No. 7 ( 2000-04-01), p. 3573-3580
    In: The Journal of Immunology, The American Association of Immunologists, Vol. 164, No. 7 ( 2000-04-01), p. 3573-3580
    Abstract: The mechanisms leading to stable T cell numbers in the periphery of a healthy animal are, to date, not well understood. We followed the expansion of CD45RBhigh (naive) and CD45RBlow (activated/memory) CD4 T cells transferred from normal mice into syngeneic Rag-20/0 recipients and the dynamics of peripheral reconstitution when both populations were coinjected. Naive cells acquired an activated phenotype and showed a high proliferative capacity that was dependent on the environment in which the recipients were kept (specific pathogen-free vs conventional housing conditions), the age of the recipients, and the presence of CD45RBlow T cells in the injected cohort. CD45RBlow CD4 T cells protected the host from CD45RBhigh CD4 T cell-induced inflammatory bowel disease and showed a limited degree of expansion. CD45RBlow CD4 T cells isolated from GF mice also showed the ability to prevent inflammatory bowel disease, indicating that at least part of the natural regulatory T cells are self-reactive. The results indicate that 1) peripheral T cell expansion in lymphocyte-deficient recipients represent classical immune responses, which are mainly promoted by exogenous Ags and 2) natural regulatory T cells control the size of the activated/memory peripheral CD4 T cell compartment.
    Type of Medium: Online Resource
    ISSN: 0022-1767 , 1550-6606
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    Language: English
    Publisher: The American Association of Immunologists
    Publication Date: 2000
    detail.hit.zdb_id: 1475085-5
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  • 2
    In: The Journal of Immunology, The American Association of Immunologists, Vol. 185, No. 2 ( 2010-07-15), p. 1196-1204
    Abstract: In many hemolytic disorders, such as malaria, the release of free heme has been involved in the triggering of oxidative stress and tissue damage. Patients presenting with severe forms of malaria commonly have impaired regulatory responses. Although intriguing, there is scarce data about the involvement of heme on the regulation of immune responses. In this study, we investigated the relation of free heme and the suppression of anti-inflammatory mediators such as PGE2 and TGF-β in human vivax malaria. Patients with severe disease presented higher hemolysis and higher plasma concentrations of Cu/Zn superoxide dismutase (SOD-1) and lower concentrations of PGE2 and TGF-β than those with mild disease. In addition, there was a positive correlation between SOD-1 concentrations and plasma levels of TNF-α. During antimalaria treatment, the concentrations of plasma SOD-1 reduced whereas PGE2 and TGF-β increased in the individuals severely ill. Using an in vitro model with human mononuclear cells, we demonstrated that the heme effect on the impairment of the production of PGE2 and TGF-β partially involves heme binding to CD14 and depends on the production of SOD-1. Aside from furthering the current knowledge about the pathogenesis of vivax malaria, the present results may represent a general mechanism for hemolytic diseases and could be useful for future studies of therapeutic approaches.
    Type of Medium: Online Resource
    ISSN: 0022-1767 , 1550-6606
    RVK:
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    Language: English
    Publisher: The American Association of Immunologists
    Publication Date: 2010
    detail.hit.zdb_id: 1475085-5
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  • 3
    In: The Journal of Immunology, The American Association of Immunologists, Vol. 186, No. 1_Supplement ( 2011-04-01), p. 106.21-106.21
    Abstract: S. mansoni infection or parasite products by induce regulatory cells and cytokines are able to down-modulate the Th1 inflammatory response involved in some autoimmune diseases. The objective of this study was to evaluate whether S. mansoni antigens are able to down-regulate the inflammatory immune response induced in vitro by the soluble Leishmania antigen (SLA) in cells of cutaneous leishmaniasis (CL) patients. Cytokines were measured in the supernatants of peripheral blood mononuclear cell (PBMC) culture stimulated with SLA in the presence and absence of S. mansoni recombinant antigens Sm29 and TSP2 and PIII, using a sandwich ELISA technique. Additionally, PBMC were evaluated for the expression of surface molecules CD14 and CD16, and also for intracellular cytokines (IL-12, TNF-alpha and IL-10). The addition of rSm29 and PIII to the cell cultures reduced the levels of IFN-γ in 54 and 58% of patients, respectively (mean reduction 49 and 56%). The three antigens used in the study were able to down modulate the production of TNF-alpha in 30% of CL patients and increased IL-10 production in 70 to 100% of them. The use of S. mansoni antigens also resulted in a lower frequency of classical and proinflammatory monocytes expressing IL-12 and TNF-alpha, while increased the frequency of monocytes expressing IL-10. The S. mansoni antigens used in this study down-modulated the inflammatory response in vitro induced by SLA in cells of CL patients.
    Type of Medium: Online Resource
    ISSN: 0022-1767 , 1550-6606
    RVK:
    RVK:
    Language: English
    Publisher: The American Association of Immunologists
    Publication Date: 2011
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  • 4
    Online Resource
    Online Resource
    The American Association of Immunologists ; 2001
    In:  The Journal of Immunology Vol. 166, No. 5 ( 2001-03-01), p. 3008-3018
    In: The Journal of Immunology, The American Association of Immunologists, Vol. 166, No. 5 ( 2001-03-01), p. 3008-3018
    Abstract: The mechanisms by which the immune system achieves constant T cell numbers throughout life, thereby controlling autoaggressive cell expansions, are to date not completely understood. Here, we show that the CD25+ subpopulation of naturally activated (CD45RBlow) CD4 T cells, but not CD25− CD45RBlow CD4 T cells, inhibits the accumulation of cotransferred CD45RBhigh CD4 T cells in lymphocyte-deficient mice. However, both CD25+ and CD25− CD45RBlow CD4 T cell subpopulations contain regulatory cells, since they can prevent naive CD4 T cell-induced wasting disease. In the absence of a correlation between disease and the number of recovered CD4+ cells, we conclude that expansion control and disease prevention are largely independent processes. CD25+ CD45RBlow CD4 T cells from IL-10-deficient mice do not protect from disease. They accumulate to a higher cell number and cannot prevent the expansion of CD45RBhigh CD4 T cells upon transfer compared with their wild-type counterparts. Although CD25+ CD45RBlow CD4 T cells are capable of expanding when transferred in vivo, they reach a homeostatic equilibrium at lower cell numbers than CD25− CD45RBlow or CD45RBhigh CD4 T cells. We conclude that CD25+ CD45RBlow CD4 T cells from nonmanipulated mice control the number of peripheral CD4 T cells through a mechanism involving the production of IL-10 by regulatory T cells.
    Type of Medium: Online Resource
    ISSN: 0022-1767 , 1550-6606
    RVK:
    RVK:
    Language: English
    Publisher: The American Association of Immunologists
    Publication Date: 2001
    detail.hit.zdb_id: 1475085-5
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  • 5
    Online Resource
    Online Resource
    The American Association of Immunologists ; 2001
    In:  The Journal of Immunology Vol. 167, No. 9 ( 2001-11-01), p. 5034-5041
    In: The Journal of Immunology, The American Association of Immunologists, Vol. 167, No. 9 ( 2001-11-01), p. 5034-5041
    Abstract: Transplants of tissues depleted of passenger leukocytes are upon in vitro culture usually accepted in allogeneic recipients. Accordingly, fully allogeneic embryonic thymic epithelium was suggested to be poorly immunogenic. However, this tissue is capable of inducing donor-specific tolerance to peripheral tissues, when restoring T cell development in nude mice, through the production of regulatory cells. In the present work, adult immunocompetent allogeneic recipients were grafted with embryonic tissues isolated at stages before hemopoietic colonization or even before the establishment of circulation. Allogeneic thymic epithelium of day 10 embryos and heart primordium of day 8 embryonic donors were always rejected. Acute rejection of the thymic anlagen takes place in less than 12 days, with maximal CD4+ and CD8+ T cell infiltrates at 10 days post-transplant. In addition, a significant infiltrate of NK1.1+ cells is observed, although without any essential role in this process. Furthermore, recipients lacking the indirect pathway of Ag presentation to CD4+ T cells do not reveal any significant delay in rejection, even when CD8+ T cells are also eliminated. Thus, our experimental approach reveals acute allograft rejection in the absence of all known pathways of naive T cell activation and therefore unveils a novel graft rejection mechanism that should be mediated by direct recognition of parenchymal cells. Given the importance of dendritic cells in naive T cell activation, it is likely that cross-reactive memory T cells may also drive rejection.
    Type of Medium: Online Resource
    ISSN: 0022-1767 , 1550-6606
    RVK:
    RVK:
    Language: English
    Publisher: The American Association of Immunologists
    Publication Date: 2001
    detail.hit.zdb_id: 1475085-5
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