B7-1 (CD80), B7-2 (CD86), interleukin-12 and transforming growth factor-beta mRNA expression in CSF and peripheral blood mononuclear cells from multiple sclerosis patients

Citation
P. Monteyne et al., B7-1 (CD80), B7-2 (CD86), interleukin-12 and transforming growth factor-beta mRNA expression in CSF and peripheral blood mononuclear cells from multiple sclerosis patients, J NEUROIMM, 91(1-2), 1998, pp. 198-203
Citations number
21
Categorie Soggetti
Neurosciences & Behavoir
Journal title
JOURNAL OF NEUROIMMUNOLOGY
ISSN journal
01655728 → ACNP
Volume
91
Issue
1-2
Year of publication
1998
Pages
198 - 203
Database
ISI
SICI code
0165-5728(19981102)91:1-2<198:B(B(IA>2.0.ZU;2-S
Abstract
Costimulatory molecules B7-1 (CD80) and B7-2 (CD86) are differently involve d in T cell stimulation. In chronic experimental autoimmune encephalomyelit is (EAE) model of multiple sclerosis (MS), B7-1 was preferentially involved in pathophysiology of relapses. We used reverse transcription polymerase c hain reaction (RT-PCR) to amplify the mRNA coding for these molecules in ce rebrospinal fluid (CSF) cells and peripheral blood mononuclear cells (PBMC) from 18 MS patients and 21 other neurological patients. In CSF cells of MS cases, B7-1 mRNA was only detected in some patients who showed clinical si gns of acute relapse at the time of the spinal tap, while B7-2 mRNA was wid ely detectable without difference between active or stable MS and controls. mRNA coding for transforming growth factor-beta (TGF-beta) was detectable in the majority of cases, with higher expression in CSF cells of MS and oth er inflammatory neurological diseases (OIND) than in noninflammatory contro ls, and higher expression in PBMC of MS patients than in all other cases. F inally, mRNA coding for interleukin (IL)-12p40 was only detected in a very few number of MS and inflammatory cases. These findings were related to pre vious detection of other cytokines in the same cases, showing relationships in CSF cells between high expression of B7-1, IL-12p40 and TNF-alpha. (C) 1998 Elsevier Science B.V. All rights reserved.