About: CCL2, but not its receptor, is essential to restrict immune privileged central nervous system‐invasion of Japanese encephalitis virus via regulating accumulation of CD11b(+) Ly‐6C(hi) monocytes

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About: CCL2, but not its receptor, is essential to restrict immune privileged central nervous system‐invasion of Japanese encephalitis virus via regulating accumulation of CD11b(+) Ly‐6C(hi) monocytes 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	CCL2, but not its receptor, is essential to restrict immune privileged central nervous system‐invasion of Japanese encephalitis virus via regulating accumulation of CD11b(+) Ly‐6C(hi) monocytes
Creator	Kim, Koanhoi Park, Sang-Youel Uyangaa, Erdenebileg Kim, Jin Choi, Jin Lee, John Eo, Seong Hossain, Altaf Kim, Seong Mohd, Ferdaus Ajit, † Patil, Mahadev
Source	Medline; PMC
abstract	Japanese encephalitis virus (JEV) is a re‐emerging zoonotic flavivirus that poses an increasing threat to global health and welfare due to rapid changes in climate and demography. Although the CCR2–CCL2 axis plays an important role in trafficking CD11b(+) Ly‐6C(hi) monocytes to regulate immunopathological diseases, little is known about their role in monocyte trafficking during viral encephalitis caused by JEV infection. Here, we explored the role of CCR2 and its ligand CCL2 in JE caused by JEV infection using CCR2‐ and CCL2‐ablated murine models. Somewhat surprisingly, the ablation of CCR2 and CCL2 resulted in starkly contrasting susceptibility to JE. CCR2 ablation induced enhanced resistance to JE, whereas CCL2 ablation highly increased susceptibility to JE. This contrasting regulation of JE progression by CCR2 and CCL2 was coupled to central nervous system (CNS) infiltration of Ly‐6C(hi) monocytes and Ly‐6G(hi) granulocytes. There was also enhanced expression of CC and CXC chemokines in the CNS of CCL2‐ablated mice, which appeared to induce CNS infiltration of these cell populations. However, our data revealed that contrasting regulation of JE in CCR2‐ and CCL2‐ablated mice was unlikely to be mediated by innate natural killer and adaptive T‐cell responses. Furthermore, CCL2 produced by haematopoietic stem cell‐derived leucocytes played a dominant role in CNS accumulation of Ly‐6C(hi) monocytes in infected bone marrow chimeric models, thereby exacerbating JE progression. Collectively, our data indicate that CCL2 plays an essential role in conferring protection against JE caused by JEV infection. In addition, blockage of CCR2, but not CCL2, will aid in the development of strategies for prophylactics and therapeutics of JE.
has issue date	2016-07-12(xsd:dateTime)
bibo:doi	10.1111/imm.12626
bibo:pmid	27260136
has license	bronze-oa
sha1sum (hex)	1b2d3f657a9e492887a83bdb1f692b2b3b1d0efc
schema:url	https://doi.org/10.1111/imm.12626
resource representing a document's title	CCL2, but not its receptor, is essential to restrict immune privileged central nervous system‐invasion of Japanese encephalitis virus via regulating accumulation of CD11b(+) Ly‐6C(hi) monocytes
has PubMed Central identifier	PMC5011677
has PubMed identifier	27260136
schema:publication	Immunology
resource representing a document's body	covid:1b2d3f657a9e492887a83bdb1f692b2b3b1d0efc#body_text
is schema:about of	named entity 'However' named entity 'CCL2' named entity 'monocyte' named entity 'CNS' named entity 'JE.' named entity 'regulation' named entity 'poses' named entity 'regulate' named entity 'innate' named entity 'models' named entity 'accumulation' named entity 'monocytes' named entity 'CCL2' named entity 'PROGRESSION' covid:arg/1b2d3f657a9e492887a83bdb1f692b2b3b1d0efc named entity 'encephalitis' named entity 'trafficking' named entity 'CCL2' named entity 'T-cell' named entity 'monocytes' named entity 'herpes simplex virus encephalitis' named entity 'host cells' named entity 'mice' named entity 'biotin' named entity 'β-actin' named entity 'flavivirus' named entity 'CCR2' named entity 'JEV' named entity 'therapeutic strategies' named entity 'leucocytes' named entity 'granulocytes' named entity 'CCL2' named entity 'CCR2' named entity 'virus' named entity 'encephalitis' named entity 'CNS' named entity 'nitric oxide' named entity 'CCR2' named entity 'CD8 +' named entity 'CCL2' named entity 'C57BL/6' named entity 'chemokines' named entity 'granulocytes' named entity 'Korea' named entity 'conjugated' named entity 'CCL2' named entity 'mice' named entity 'CCL2' named entity 'CD11b' named entity 'infection' named entity 'CD4 +' named entity 'myeloid' named entity 'antigen' named entity 'spleen' named entity 'T-cell' named entity 'CCL2' named entity 'Oslo' named entity 'monocytes' named entity 'infection' named entity 'KO mice' named entity 'TNF' named entity 'bone marrow' named entity 'JEV' named entity 'HSCs' named entity 'CD11b' named entity 'CD11b' named entity 'granulocytes' named entity 'inflammatory reactions' named entity 'JEV' named entity 'CCL2'

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