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Protein Kinase A RI Subunit Deficiency in Lupus T Lymphocytes: Bypassing a Block in RI Translation Reconstitutes Protein Kinase A Activity and Augments IL-2 Production¹

Section on Rheumatology and Clinical Immunology, Department of Internal Medicine, Wake Forest University School of Medicine, Winston-Salem, NC 27157

A profound deficiency of type I protein kinase A (PKA-I or RI/₂C₂) phosphotransferase activity occurs in the T lymphocytes of 80% of subjects with systemic lupus erythematosus (SLE), an autoimmune disorder of unknown etiology. This isozyme deficiency is predominantly the product of reduced or absent isoform of the type I regulatory subunit (RI). Transient transfection of RI cDNAs from SLE subjects into autologous T cells that do not synthesize the RI subunit bypassed the block, resulting in RI subunit synthesis and restoration of the PKA-I (RI₂C₂) holoenzyme. Transfected T cells activated via the T cell surface receptor complex revealed a significant increase of cAMP-activatable PKA activity that was associated with a significant increase in IL-2 production. These data demonstrate that a disorder of RI translation exists, and that correction of the PKA-I deficiency may enhance T lymphocyte effector functions in SLE.

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