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  Vol. 62 No. 5, May 2005 TABLE OF CONTENTS
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Kinin B1 Receptor Expression on Multiple Sclerosis Mononuclear Cells

Correlation With Magnetic Resonance Imaging T2-Weighted Lesion Volume and Clinical Disability

Alexandre Prat, MD, PhD, FRCPC; Katarzyna Biernacki, PhD; Tanya Saroli, MD; John E. Orav, PhD; Charles R. G. Guttmann, MD; Howard L. Weiner, MD; Samia J. Khoury, MD; Jack P. Antel, MD

Arch Neurol. 2005;62:795-800.

Background  We have previously shown that the inducible kinin B1 receptor is expressed on T lymphocytes during relapses and progression in multiple sclerosis.

Objective  To evaluate the correlation between the expression of B1 receptor on peripheral blood mononuclear cells derived from patients who have multiple sclerosis with serial, clinical magnetic resonance imaging and immunological study–derived measures.

Design  Using frozen samples obtained from a high-frequency magnetic resonance imaging–immunological study, we analyzed B1 receptor messenger RNA (mRNA) expression in peripheral blood–derived mononuclear cells serially collected from 6 patients with multiple sclerosis and 8 healthy control subjects by semiquantitative radioactive duplex reverse transcriptase–polymerase chain reaction amplification. Time-course kinin B1–actin mRNA ratios were subsequently compared with corresponding clinical magnetic resonance imaging and immune parameters.

Results  The time-course kinin B1–actin mRNA ratio correlated positively with the Expanded Disability Status Scale index (P<.001), occurrence of clinical relapse (P = .02), volume of lesion on T2-weighted images (P<.003) and interleukin 2 receptor and major histocompatibility complex class II expression on CD4+ lymphocytes, but not with gadolinium-enhancing lesions. The time-course kinin B1–actin mRNA ratios were 5 to 25 times lower in samples derived from healthy controls.

Conclusion  The correlation of kinin B1 receptor mRNA levels with dynamic clinical and magnetic resonance imaging measures suggests that expression of this receptor can serve as an index of disease activity in multiple sclerosis.


Author Affiliations: Neuroimmunology Unit, Montréal Neurological Institute, McGill University, Montréal, Québec (Drs Prat, Biernacki, Saroli, and Antel); Department of Clinical Epidemiology (Dr Orav) and the Center for Neurologic Diseases, Brigham and Women’s Hospital (Drs Guttmann, Weiner, and Khoury), Harvard Medical School, Boston, Mass. Dr Prat is now with the Multiple Sclerosis Clinic and Neuroimmunology Laboratory, Centre Hospitalier de l’Université de Montréal–Hôpital Notre-Dame.







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