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Chemokines in neurological disease models: correlation between chemokine expression patterns and inflammatory pathology
Author(s) -
Ransohoff Richard M.
Publication year - 1997
Publication title -
journal of leukocyte biology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.819
H-Index - 191
eISSN - 1938-3673
pISSN - 0741-5400
DOI - 10.1002/jlb.62.5.645
Subject(s) - chemokine , chemokine receptor , biology , ccl17 , inflammation , immunology , ccr10 , ccl13 , ccl18 , ccr1 , immune system
We have recently determined chemokine expression profiles in a variety of models of neural trauma and immune‐inflammation. The results indicate the following: (1) Chemokine expression in posttraumatic inflammation is generally restricted to the monocyte chemoattractant MCP‐1, and occurs before hematogenous cell entry into neural tissues. Therefore MCP‐1 is an excellent candidate for a mediator of leukocyte recruitment in these settings. (2) Chemokine expression in immune‐inflammation is diverse and includes both α‐ and β‐chemokines. Chemokine production can be attributed to parenchymal and infiltrating cell populations. Early signs of inflammation precede chemokine expression, which is believed to exert the crucial function of amplifying the immunemediated inflammatory reaction. These observations provide a basis for evaluating model neurological disorders in transgenic mice that express chemokines ectopically or in mice that are deficient in chemokine ligands or receptors as a consequence of gene targeting. Ultimately, a clear definition of roles of chemokines and their receptors in neurological diseases will suggest rational intervention. J. Leukoc. Biol. 62: 645–652; 1997.