About: A Critical Blimp-1-Dependent IL-10 Regulatory Pathway in T Cells Protects From a Lethal Pro-inflammatory Cytokine Storm During Acute Experimental Trypanosoma brucei Infection

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About: A Critical Blimp-1-Dependent IL-10 Regulatory Pathway in T Cells Protects From a Lethal Pro-inflammatory Cytokine Storm During Acute Experimental Trypanosoma brucei Infection Goto Sponge NotDistinct Permalink

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Attributes	Values
type	Academic Article research paper schema:ScholarlyArticle
isDefinedBy	Covid-on-the-Web dataset
has title	A Critical Blimp-1-Dependent IL-10 Regulatory Pathway in T Cells Protects From a Lethal Pro-inflammatory Cytokine Storm During Acute Experimental Trypanosoma brucei Infection
Creator	Caljon, Guy De Trez, Carl Magez, Stefan Boon, Louis Humphreys, Ian Franco, Manuel Snick, Jacques Bockstal, Viki Cnops, Jennifer Kline, Glaxo-Smith Korf, Hannelie Lauvau, Gregoire Muraille, Eric Stijlemans, Benoit Van Ginderachter, Jo
Source	PMC
abstract	In many infectious diseases, the immune response operates as a double-edged sword. While required for protective immunity, infection-induced inflammation can be detrimental if it is not properly controlled, causing collateral body damage and potentially leading to death. It is in this context that the potent anti-inflammatory cytokine interleukin-10 (IL-10) is required to dampen the pro-inflammatory immune response that hallmarks trypanosomosis. Effective control of this infection requires not just the action of antibodies specific for the parasite's variable surface glycoprotein (VSG) coat antigens, but also a pro-inflammatory immune response mediated mainly by IFNγ, TNF, and NO. However, strict control of inflammation is mandatory, as IL-10-deficient mice succumb from an unrestrained cytokine storm within 10 days of a Trypanosome brucei infection. The relevant cellular source of IL-10 and the associated molecular mechanisms implicated in its trypanosomosis associated production are poorly understood. Using an IL-10 reporter mouse strain (Vert-X), we demonstrate here that NK cells, CD8(+) T cells and CD4(+) T cells as well as B cells and plasma cells constitute potential cellular sources of IL-10 within the spleen and liver during acute infection. The IL-10 wave follows peak pro-inflammatory cytokine production, which accompanied the control of peak parasitemia. Similar results were observed following conventional experimental needle infection and physiological infections via T. brucei-infected tsetse flies. Our results show that conditional T cell-specific ablation of the IL-10 regulating Prdm1 gene (encoding for the Blimp-1 transcription factor), leads to an uncontrolled trypanosome-induced pro-inflammatory syndrome like the one observed in infected IL-10-deficient mice. This result indicates that the biological role of IL-10-derived from non-T cells, including NK cells, is of minor importance when considering host survival. The cytokine IL-27 that is also considered to be an IL-10 regulator, did not affect IL-10 production during infection. Together, these data suggest that T. brucei activates a Blimp-1-dependent IL-10 regulatory pathway in T cells that acts as a critical anti-inflammatory rheostat, mandatory for host survival during the acute phase of parasitemia.
has issue date	2020-06-04(xsd:dateTime)
bibo:doi	10.3389/fimmu.2020.01085
has license	cc-by
sha1sum (hex)	cb171f3e557a828685bc9a702e1315bacb3d140a
schema:url	https://doi.org/10.3389/fimmu.2020.01085
resource representing a document's title	A Critical Blimp-1-Dependent IL-10 Regulatory Pathway in T Cells Protects From a Lethal Pro-inflammatory Cytokine Storm During Acute Experimental Trypanosoma brucei Infection
has PubMed Central identifier	PMC7325990
schema:publication	Front Immunol
resource representing a document's body	covid:cb171f3e557a828685bc9a702e1315bacb3d140a#body_text
is schema:about of	named entity 'clone' named entity 'infection' named entity 'cytokine storm' named entity 'IL-27' named entity 'IL-10' named entity 'mice' named entity 'Pro-inflammatory Cytokine' named entity 'IL-10' named entity 'IgG2a' named entity 'IL-10' named entity 'glycerol' named entity 'mice' named entity 'parasites' named entity 'cell type' named entity 'infection' named entity 'intracellular' named entity 'blood sampling' named entity 'T. brucei' named entity 'IL-6' named entity 'infection' named entity 'variable surface glycoprotein' named entity 'trypanosomes' named entity 'antibiotic' named entity 'CD8 +' named entity 'immunopathology' named entity 'T. brucei' named entity 'Il10' named entity 'Blimp-1' named entity 'trypanosomosis' named entity 'infection' named entity 'mice' named entity 'inflammation' named entity 'infection' named entity 'IL-10' named entity 'parasites' named entity 'T. brucei' named entity 'infection' named entity 'parasites' named entity 'T. brucei' named entity 'gene' named entity 'T. brucei' named entity 'CD11a' named entity 'effector' named entity 'CD11a' named entity 'IL-10' named entity 'IL-10' named entity 'trypanosome' named entity 'cell cultures' named entity 'T-bet' named entity 'Cytokine' named entity 'gene' named entity 'liver cells' named entity 'type 1' named entity 'IL-10' named entity 'Gosselies' named entity 'clone' named entity 'inflammation' named entity 'hematopoietic' named entity 'IL-10' named entity 'IFNγ' named entity '0.01' named entity 'NK cells' named entity 'liver' named entity 'Prdm1' named entity 'NK1.1' named entity 'mouse strain' named entity 'Blimp-1' named entity 'IL-10' named entity 'infection'

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