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Elevated serum and CSF levels of soluble CD30 during clinical remission in multiple sclerosis

From the Regional Immunology Service (Dr. McMillan and J.P. Douglas), Royal Group of Hospitals; the Northern Ireland Neurology Service (Drs. McDonnell, Droogan, and Hawkins), Royal Group of Hospitals; and the School of Clinical Medicine (Dr. Hawkins), The Queen's University of Belfast, Northern Ireland. Dr. McDonnell has been a Research Fellow at the Royal Victoria Hospital, Belfast.

Address correspondence and reprint requests to Dr McMillan, Regional Immunology Service, Royal Group of Hospitals, Belfast, Northern Ireland, BT12 6BN.

Objective: To ascertain the presence of the Th2 response in MS patients by evaluating the level of soluble (s) CD30 across the clinical spectrum of MS and during relapse and remission.

Background: MS is considered a T-cell-mediated disorder with the immune attack dominated by a Th1 cytokine response. Elevated levels of sCD30 have been associated with CD4⁺ cells that secrete Th2-type cytokines.

Methods: Levels of sCD30 were determined in the serum and CSF of patients with primary progressive MS, secondary progressive MS, relapsing-remitting MS (RRMS), both in relapse and remission, and in patients with other inflammatory neurologic disease (IND) and noninflammatory neurologic disease (NIND). None of the patients were on immunomodulatory treatment.

Results: Higher serum levels of sCD30 were detected in all MS subgroups and IND patients compared with NIND patients. RRMS patients in remission had significantly higher levels than those in relapse (median, 45.7 U/mL versus 18.3 U/mL; p = 0.04). Significantly higher CSF levels were also found in all groups, except those with RRMS in relapse compared with NIND patients. Again, RRMS patients in remission had higher CSF sCD30 levels compared with those in relapse (median, 4.0 U/mL versus 3.0 U/mL; p = 0.08).

Conclusions: Serum and CSF levels of sCD30 are increased in MS, particularly during remission. The results provide additional evidence for the presence of a Th2 response and indicate that sCD30 may be of value as a marker of lesion resolution.

Received December 5, 1997. Accepted in final form June 27, 1998.

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