About: Enhanced CD8 T-cell anti-viral function and clinical disease in B7-H1-deficient mice requires CD4 T cells during encephalomyelitis

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About: Enhanced CD8 T-cell anti-viral function and clinical disease in B7-H1-deficient mice requires CD4 T cells during encephalomyelitis Goto Sponge NotDistinct Permalink

An Entity of Type : schema:ScholarlyArticle, within Data Space : covidontheweb.inria.fr associated with source document(s)

Attributes	Values
type	Academic Article research paper schema:ScholarlyArticle
isDefinedBy	Covid-on-the-Web dataset
has title	Enhanced CD8 T-cell anti-viral function and clinical disease in B7-H1-deficient mice requires CD4 T cells during encephalomyelitis
Creator	Bergmann, Cornelia Hinton, David Phares, Timothy Stohlman, Stephen
Source	Medline; PMC
abstract	BACKGROUND: Anti-viral CD8 T-cell activity is enhanced and prolonged by CD4 T-cell-mediated help, but negatively regulated by inhibitory B7-H1 interactions. During viral encephalomyelitis, the absence of CD4 T cells decreases CD8 T cell activity and impedes viral control in the central nervous system (CNS). By contrast, the absence of B7-H1 enhances CD8 T-cell function and accelerates viral control, but increases morbidity. However, the relative contribution of CD4 T cells to CD8 function in the CNS, in the absence of B7-H1, remains unclear. METHODS: Wild-type (WT) and B7-H1(−/−) mice were infected with a gliatropic coronavirus and CD4 T cells depleted to specifically block T helper function in the CNS. Flow cytometry and gene expression analysis of purified T-cell populations from lymph nodes and the CNS was used to directly monitor ex vivo T-cell effector function. The biological affects of altered T-cell responses were evaluated by analysis of viral control and spinal-cord pathology. RESULTS: Increased anti-viral activity by CD8 T cells in the CNS of B7-H1(−/−) mice was lost upon depletion of CD4 T cells; however, despite concomitant loss of viral control, the clinical disease was less severe. CD4 depletion in B7-H1(−/−) mice also decreased inducible nitric oxide synthase expression by microglia and macrophages, consistent with decreased microglia/macrophage activation and reduced interferon (IFN)-γ. Enhanced production of IFN-γ, interleukin (IL)-10 and IL-21 mRNA was seen in CD4 T cells from infected B7-H1(−/−) compared with WT mice, suggesting that over-activated CD4 T cells primarily contribute to the increased pathology. CONCLUSIONS: The local requirement of CD4 T-cell help for CD8 T-cell function is not overcome if B7-H1 inhibitory signals are lost. Moreover, the increased effector activity by CD8 T cells in the CNS of B7-H1(−/−) mice is attributable not only to the absence of B7-H1 upregulation on major histocompatibility complex class I-presenting resident target cells, but also to enhanced local CD4 T-cell function. B7-H1-mediated restraint of CD4 T-cell activity is thus crucial to dampen both CD8 T-cell function and microglia/macrophage activation, thereby providing protection from T-cell-mediated bystander damage.
has issue date	2012-12-14(xsd:dateTime)
bibo:doi	10.1186/1742-2094-9-269
bibo:pmid	23237504
has license	cc-by
sha1sum (hex)	c59d6e789176b928523129adb96ca495720a3b4a
schema:url	https://doi.org/10.1186/1742-2094-9-269
resource representing a document's title	Enhanced CD8 T-cell anti-viral function and clinical disease in B7-H1-deficient mice requires CD4 T cells during encephalomyelitis
has PubMed Central identifier	PMC3545890
has PubMed identifier	23237504
schema:publication	J Neuroinflammation
resource representing a document's body	covid:c59d6e789176b928523129adb96ca495720a3b4a#body_text
is schema:about of	named entity 'altered' named entity 'activity' named entity 'ENHANCED' named entity 'DISEASE' named entity 'ALTERED' named entity 'CNS' named entity 'CONTROL' named entity 'RESPONSES' named entity 'B7-H1' named entity 'DEPLETED' named entity 'MICE' named entity 'T CELLS' named entity 'ACCELERATES' named entity 'GENE EXPRESSION ANALYSIS' named entity 'T HELPER' named entity 'INHIBITORY' named entity 'ANALYSIS' named entity 'REGULATED' named entity 'INCREASES' named entity 'EFFECTOR' named entity 'DECREASES' named entity 'LYMPH NODES' named entity 'T-CELL' named entity 'CENTRAL NERVOUS SYSTEM' named entity 'CD8' named entity 'INTERACTIONS' named entity 'ABSENCE OF' named entity 'EX VIVO' named entity 'PURIFIED' named entity 'BIOLOGICAL' named entity 'MEDIATED' named entity 'CONTRIBUTION' named entity 'PATHOLOGY' named entity 'CORONAVIRUS' named entity 'USED' named entity 'PROLONGED' named entity 'T CELL' named entity 'VIRAL' named entity 'B7-H1' named entity 'T CELLS' named entity 'VIRAL FUNCTION' named entity 'CD4' named entity 'FUNCTION' named entity 'INFECTED' named entity 'MICE' named entity 'ENCEPHALOMYELITIS' named entity 'CD8' named entity 'CLINICAL' named entity 'T-CELL' named entity 'FLOW CYTOMETRY' named entity 'ENCEPHALOMYELITIS' named entity 'DIRECTLY' named entity 'CD4' named entity 'HELP' named entity 'BACKGROUND' named entity 'CONTRAST' named entity 'SPINAL-CORD' named entity 'WILD-TYPE' named entity 'RELATIVE' named entity 'BLOCK' named entity 'MONITOR' named entity 'BUT' named entity 'POPULATIONS' named entity 'DEFICIENT' named entity 'CELL ACTIVITY' named entity 'UNCLEAR' named entity 'CELL FUNCTION' named entity 'ENHANCED' named entity 'METHODS' named entity 'EVALUATED' named entity 'MORBIDITY' covid:arg/c59d6e789176b928523129adb96ca495720a3b4a named entity 'responses' named entity 'T cell' named entity 'B7-H1' named entity 'vivo' named entity 'B7-H1' named entity 'viral'

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