Please use this identifier to cite or link to this item:
https://hdl.handle.net/2440/39273
Citations | ||
Scopus | Web of Science® | Altmetric |
---|---|---|
?
|
?
|
Full metadata record
DC Field | Value | Language |
---|---|---|
dc.contributor.author | McColl, S. | - |
dc.contributor.author | Mahalingam, S. | - |
dc.contributor.author | Staykova, M. | - |
dc.contributor.author | Tylaska, L. | - |
dc.contributor.author | Fisher, K. | - |
dc.contributor.author | Strick, C. | - |
dc.contributor.author | Gladue, R. | - |
dc.contributor.author | Neote, K. | - |
dc.contributor.author | Willenborg, D. | - |
dc.date.issued | 2004 | - |
dc.identifier.citation | Laboratory Investigation, 2004; 84(11):1418-1429 | - |
dc.identifier.issn | 0023-6837 | - |
dc.identifier.issn | 1530-0307 | - |
dc.identifier.uri | http://hdl.handle.net/2440/39273 | - |
dc.description | © 2007 United States and Canadian Academy of Pathology | - |
dc.description.abstract | The chemokines are a large gene superfamily with critical roles in development and immunity. The chemokine receptor CXCR3 appears to play a major role in the trafficking of activated Th1 lymphocytes. There are at least three major ligands for CXCR3: mig/CXCL9, IP-10/CXCL10 and I-TAC/CXCL11, and of these three ligands, CXCL11 is the least well-characterized. In this study, we have cloned a rat ortholog of CXCL11, evaluated its function, and examined its expression in the Th-1-mediated disease, experimental autoimmune encephalomyelitis (EAE) in the rat. Based on its predicted primary amino-acid sequence, rat I-TAC/CXCL11 was synthesized and shown to induce chemotaxis of activated rat T lymphocytes in vitro and the in vivo migration of T lymphocytes when injected into the skin. I-TAC/CXCL11 expression, as determined by RT-PCR, increased in lymph node and spinal cord tissue collected from rats in which EAE had been actively induced, and in spinal cord tissue from rats in which EAE had been passively induced. The kinetics of expression were similar to that of CXCR3 and IP-10/CXCL10, although expression of both CXCR3 and IP-10/CXCL10 was more intense than that of I-TAC/CXCL11 and increased more rapidly in both lymph nodes and the spinal cord. Only minor levels of expression of the related chemokine mig/CXCL9 were observed. Immunohistochemistry revealed that the major cellular source of I-TAC/CXCL11 in the central nervous system (CNS) during EAE is likely to be the astrocyte. Together, these data indicate that I-TAC/CXCL11 is expressed in the CNS during the clinical phase of EAE. However, the observation that I-TAC/CXCL11 is expressed after receptor expression is detected suggests that it is not essential for the initial migration of CXCR3-bearing cells into the CNS. | - |
dc.description.statementofresponsibility | Shaun R McColl, Surendran Mahalingam, Maria Staykova, Laurie A Tylaska, Katherine E Fisher, Christine A Strick, Ronald P Gladue, Kuldeep S Neote and David O Willenborg | - |
dc.language.iso | en | - |
dc.publisher | Nature Publishing Group | - |
dc.source.uri | http://www.nature.com/labinvest/journal/v84/n11/full/3700155a.html | - |
dc.subject | Lymph Nodes | - |
dc.subject | Spleen | - |
dc.subject | T-Lymphocytes | - |
dc.subject | Cells, Cultured | - |
dc.subject | Animals | - |
dc.subject | Rats, Inbred Lew | - |
dc.subject | Humans | - |
dc.subject | Rats | - |
dc.subject | Encephalomyelitis, Autoimmune, Experimental | - |
dc.subject | Disease Models, Animal | - |
dc.subject | Receptors, Chemokine | - |
dc.subject | RNA, Messenger | - |
dc.subject | Chemokines, CC | - |
dc.subject | Chemokines, CXC | - |
dc.subject | Ligands | - |
dc.subject | Cloning, Molecular | - |
dc.subject | Reverse Transcriptase Polymerase Chain Reaction | - |
dc.subject | Chemotaxis | - |
dc.subject | Amino Acid Sequence | - |
dc.subject | Dose-Response Relationship, Drug | - |
dc.subject | Molecular Sequence Data | - |
dc.subject | Female | - |
dc.subject | Receptors, CXCR3 | - |
dc.subject | Chemokine CXCL11 | - |
dc.subject | Chemokine CCL11 | - |
dc.title | Expression of rat I-TAC/CXCL11/SCYA11 during central nervous system inflammation: comparison with other CXCR3 ligands | - |
dc.type | Journal article | - |
dc.identifier.doi | 10.1038/labinvest.3700155 | - |
pubs.publication-status | Published | - |
dc.identifier.orcid | McColl, S. [0000-0003-0949-4660] | - |
Appears in Collections: | Aurora harvest 6 Microbiology and Immunology publications |
Files in This Item:
There are no files associated with this item.
Items in DSpace are protected by copyright, with all rights reserved, unless otherwise indicated.