Impaired mobility of human t lymphocyte surface molecules during inactive systemic lupus erythematosus. relationship to a defective camp pathway
Corresponding Author
Gary M. Kammer MD
Associate Professor of Medicine
Division of Rheumatic Diseases, Department of Medicine, Case Western Reserve University School of Medicine, Cleveland, Ohio.
Address reprints requests to Gary M. Kammer, MD, Department of Medicine, 2074 Abington Road, Cleveland, OH 44106Search for more papers by this authorElizabeth Mitchell BS
Medical Student
Division of Rheumatic Diseases, Department of Medicine, Case Western Reserve University School of Medicine, Cleveland, Ohio.
Search for more papers by this authorCorresponding Author
Gary M. Kammer MD
Associate Professor of Medicine
Division of Rheumatic Diseases, Department of Medicine, Case Western Reserve University School of Medicine, Cleveland, Ohio.
Address reprints requests to Gary M. Kammer, MD, Department of Medicine, 2074 Abington Road, Cleveland, OH 44106Search for more papers by this authorElizabeth Mitchell BS
Medical Student
Division of Rheumatic Diseases, Department of Medicine, Case Western Reserve University School of Medicine, Cleveland, Ohio.
Search for more papers by this authorAbstract
The T lymphocytes of patients with active systemic lupus erythematosus (SLE) exhibit impaired capping of the surface molecules CD3, CD4, and CD8 and a defective cAMP-dependent pathway. Since the mobility of these molecules is regulated in part by cAMP, we sought to determine whether there is a specific defect(s) along the T cell cAMP pathway that contributes to the persistent capping disorder observed during inactive SLE. The data suggest that a defect may exist at the level of cAMP-dependent protein kinase activation or at a point distally. We propose that a disorder of cAMP-dependent protein kinase activity might account for the defect of capping observed in both the CD3, CD4 (helper/inducer) and CD3,CD8 (suppressor) subsets observed in SLE.
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