We are analyzing https://link.springer.com/article/10.1186/jbiol34.

Title:
Suppression of adaptive immunity to heterologous antigens during Plasmodium infection through hemozoin-induced failure of dendritic cell function | Journal of Biology
Description:
Background Dendritic cells (DCs) are central to the initiation and regulation of the adaptive immune response during infection. Modulation of DC function may therefore allow evasion of the immune system by pathogens. Significant depression of the host
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Keywords {🔍}

cells, dcs, pubmed, google, scholar, article, cas, malaria, infection, mice, figure, uninfected, infected, tcell, erythrocytes, function, vitro, plasmodium, immune, vivo, chabaudi, response, lps, activation, ovaspecific, cell, immunol, results, parasite, prbcs, suppression, dendritic, chabaudiinfected, immunity, responses, immunized, parasites, central, maturation, expression, reduced, blood, levels, falciparum, open, studies, antigen, shown, days, antigenspecific,

Topics {✒️}

cd8+/hla-dq-restricted suppressor cells peroxisome proliferator-activated receptor-γ major histocompatibility complex circulating epstein-barr virus-carrying ova-specific t-cell receptor-transgenic mitogen-stimulated t-cell cytokines molecule hla-dr compared article download pdf t-cell-antigen-receptor-transgenic stimulated bone-marrow-derived dcs 6-carboxy-succinimidyl-fluorescein ester uv-visible helios spectrophotometer bone-marrow-derived dcs cultured nf-κb-dependent pathways transferred b-cell-receptor transgenic myd88-dependent signaling pathway chabaudi-derived membrane-expressed proteins reverse light/dark cycle cd4+cd8+tcrlo thymocytes laser-scanning cytometer equipped parasite-derived immunosuppressive factor public-health problems resulting hen egg-white lysozyme extracellular signal-regulated kinase hemozoin-inducible proinflammatory events optimal t-cell response inducible il-12p40 subunit bone-marrow-derived dcs epstein-barr virus-infected bone-marrow cell concentration optimal t-cell expansion stimulate t-cell proliferation defective t-cell control schizont-infected rhesus erythrocytes identify b-cell areas large-scale vaccine regimes induce t-cell proliferation parasites express 'neo-proteins' t-cell proliferative response endogenous malarial antigen-specific blood-borne parasite antigens leaves malaria-infected individuals defective b-cell expansion antigen-presenting cell function pro-inflammatory cytokines caused cd4+ t-cell function ova-specific serum immunoglobulin cd4+ t-cell migration specific pathogen-free conditions cd4+ t-cell expansion

Questions {❓}

Riley EM: Is T-cell priming required for initiation of pathology in malaria infections?

Schema {🗺️}

WebPage:
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         headline:Suppression of adaptive immunity to heterologous antigens during Plasmodium infection through hemozoin-induced failure of dendritic cell function
         description:Dendritic cells (DCs) are central to the initiation and regulation of the adaptive immune response during infection. Modulation of DC function may therefore allow evasion of the immune system by pathogens. Significant depression of the host's systemic immune response to both concurrent infections and heterologous vaccines has been observed during malaria infection, but the mechanisms underlying this immune hyporesponsiveness are controversial. Here, we demonstrate that the blood stages of malaria infection induce a failure of DC function in vitro and in vivo, causing suboptimal activation of T cells involved in heterologous immune responses. This effect on T-cell activation can be transferred to uninfected recipients by DCs isolated from infected mice. Significantly, T cells activated by these DCs subsequently lack effector function, as demonstrated by a failure to migrate to lymphoid-organ follicles, resulting in an absence of B-cell responses to heterologous antigens. Fractionation studies show that hemozoin, rather than infected erythrocyte (red blood cell) membranes, reproduces the effect of intact infected red blood cells on DCs. Furthermore, hemozoin-containing DCs could be identified in T-cell areas of the spleen in vivo. Plasmodium infection inhibits the induction of adaptive immunity to heterologous antigens by modulating DC function, providing a potential explanation for epidemiological studies linking endemic malaria with secondary infections and reduced vaccine efficacy.
         datePublished:2006-04-12T00:00:00Z
         dateModified:2006-04-12T00:00:00Z
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            Major Histocompatibility Complex Class
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            Uninfected Mouse
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      headline:Suppression of adaptive immunity to heterologous antigens during Plasmodium infection through hemozoin-induced failure of dendritic cell function
      description:Dendritic cells (DCs) are central to the initiation and regulation of the adaptive immune response during infection. Modulation of DC function may therefore allow evasion of the immune system by pathogens. Significant depression of the host's systemic immune response to both concurrent infections and heterologous vaccines has been observed during malaria infection, but the mechanisms underlying this immune hyporesponsiveness are controversial. Here, we demonstrate that the blood stages of malaria infection induce a failure of DC function in vitro and in vivo, causing suboptimal activation of T cells involved in heterologous immune responses. This effect on T-cell activation can be transferred to uninfected recipients by DCs isolated from infected mice. Significantly, T cells activated by these DCs subsequently lack effector function, as demonstrated by a failure to migrate to lymphoid-organ follicles, resulting in an absence of B-cell responses to heterologous antigens. Fractionation studies show that hemozoin, rather than infected erythrocyte (red blood cell) membranes, reproduces the effect of intact infected red blood cells on DCs. Furthermore, hemozoin-containing DCs could be identified in T-cell areas of the spleen in vivo. Plasmodium infection inhibits the induction of adaptive immunity to heterologous antigens by modulating DC function, providing a potential explanation for epidemiological studies linking endemic malaria with secondary infections and reduced vaccine efficacy.
      datePublished:2006-04-12T00:00:00Z
      dateModified:2006-04-12T00:00:00Z
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         Major Histocompatibility Complex Class
         Malaria Infection
         Infected Erythrocyte
         Uninfected Mouse
         Life Sciences
         general
         Biomedicine
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