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NEUROLOGY 1998;51:753-758
© 1998 American Academy of Neurology

Increased release of interleukin-12p40 in MS

Association with intracerebral inflammation

K. Fassbender, MD, A. Ragoschke, S. Rossol, MD, A. Schwartz, MD, O. Mielke, MD, A. Paulig and M. Hennerici, MD

From the Department of Neurology (Drs. Fassbender, Schwartz, Mielke, and Hennerici, and A. Ragoschke and A. Paulig) and Internal Medicine (Dr. Rossol), University of Heidelberg, Klinikum Mannheim, Germany.

Address correspondence and reprint requests to Dr. Klaus Fassbender, Department of Neurology, Klinikum Mannheim, University of Heidelberg, Theodor-Kutzer-Ufer, D-68135 Mannheim, Germany.

Objective: The p40 subunit of interleukin (IL)-12 was recently demonstrated in active lesions in MS. We tested whether the p40 subunit of IL-12 can also be detected in CSF and serum of patients with this disease and, if so, whether release is associated with inflammatory disease activity.

Results: This study demonstrates an increased (up to 1,000-fold) compartmentalized release of the p40 subunit but not of the heterodimer p70 in MS. Release of IL-12p40 correlated with classic markers of CNS inflammation (CSF cell counts, immunoglobulin G index) and was significantly increased in patients with gadolinium-enhancing plaques on MRI. Moreover, release of IL-12p40 was associated with CSF levels of myelin basic protein as a measure of myelin degradation.

Conclusion: These results suggest a role of IL-12p40 in the pathophysiology of MS.


Supported by the Forschungsfond Mannheim, University of Heidelberg.

Received November 24, 1997. Accepted in final form May 5, 1998.




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