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NEUROLOGY 1992;42:1609
© 1992 American Academy of Neurology

Expression of monocyte activation antigen Mo3 on the surface of peripheral blood monocytes from patients with multiple sclerosis

Paula Dore-Duffy, PhD, Carol Donovan, BS and Robert F. Todd, III, MD, PhD

Multiple Sclerosis Clinical and Research Center (Dr. Dore-Duffy and C. Donovan), Department of Neurology, Wayne State University School of Medicine, Detroit, MI; and the Simpson Memorial Research Institute (Dr. Todd), Division of Hematology/Oncology, Department of Internal Medicine, University of Michigan Medical School, Ann Arbor, MI.

Exposure of human peripheral blood monocytes (PBM) to phorbol esters, bacterial products, and cyclic adenosine monophosphate agonists is known to stimulate expression of a plasma membrane antigen ([Ag]; Mo3). Mo3 is recognized by two monoclonal antibodies, Mo3e (IgM), and Mo3f (IgG). Surface Mo3 is barely detectable by indirect immunofluorescence flow cytometry in nonstimulated monocytes. Mo3-positive monocytes have been found in inflammatory tissues, but increased surface expression of Mo3 in PBM has not been seen in any patient group. We report that PBM from patients with chronic progressive MS (CPMS) express increased Mo3. PBM from patients with other neurologic diseases and healthy controls express little measurable Mo3. No difference was seen in class II major histocompatibility complex Ag expression and in Mo2 (CD14) expression. Exposure of PBM to lipopolysaccharide (10 mg/ml) enhanced Mo3 expression in both MS patients and controls. Mo3 expression on CPMS PBM was not dependent on culture conditions. Taken together, our observations suggest that monocytes from patients with MS are stimulated in vivo to express activation Ag Mo3, but that Mo3-positive monocytes need not be upregulated for HLA-DR.

Address correspondence and reprint requests to Dr. Paula Dore-Duffy, Department of Neurology, 6 E UHC, Wayne State University, Detroit, MI 48201.

Supported in part by a grant from the National Multiple Sclerosis Society and grant CA 42246 from the National Institutes of Health.

Received October 22, 1991. Accepted for publication in final form January 3, 1992.




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