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Expression of the interferon‐γ‐inducible chemokines IP‐10 and Mig and their receptor, CXCR3, in multiple sclerosis lesions
Author(s) -
Simpson J. E.,
Newcombe J.,
Cuzner M. L.,
Woodroofe M. N.
Publication year - 2000
Publication title -
neuropathology and applied neurobiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.538
H-Index - 95
eISSN - 1365-2990
pISSN - 0305-1846
DOI - 10.1046/j.1365-2990.2000.026002133.x
Subject(s) - cxcr3 , multiple sclerosis , chemokine receptor , interferon , chemokine , receptor , medicine , immunology , cancer research
The recruitment of leucocytes to sites of inflammation is an important feature of multiple sclerosis (MS) pathology. Chemokines are involved in the activation and specific directional migration of monocytes and T‐lymphocytes to sites of inflammation. Using immunocytochemistry, the expression of the α‐chemokines, interferon (IFN)‐γ‐inducible protein‐10 (IP‐10) and monokine induced by IFN‐γ (Mig), and their receptor CXCR3 have been examined in post‐mortem central nervous system (CNS) tissue from MS cases at different stages of lesion development. In actively demyelinating lesions both IP‐10 and Mig protein were predominantly expressed by macrophages within the plaque and by reactive astrocytes in the surrounding parenchyma. CXCR3 was expressed by T cells and by astrocytes within the plaque. Interferon‐γ may stimulate glial cells to express IP‐10 and Mig, which continue the local inflammatory response by selectively recruiting activated T‐lymphocytes into the CNS.