The role of protein kinase C isoenzymes in the pathogenesis of human autoimmune diseases
The physiological role of protein kinase C (PKC) enzymes in the immune system is presented briefly. From earlier publications of others data were collected how the defects of one/two isoenzymes of PKC system suggested their involvement in the pathogenesis of human autoimmune diseases. Our observatio...
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Published in | Clinical immunology (Orlando, Fla.) Vol. 241; p. 109071 |
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Main Authors | , , , , , , |
Format | Journal Article |
Language | English |
Published |
Elsevier Inc
01.08.2022
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Subjects | |
Online Access | Get full text |
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Summary: | The physiological role of protein kinase C (PKC) enzymes in the immune system is presented briefly. From earlier publications of others data were collected how the defects of one/two isoenzymes of PKC system suggested their involvement in the pathogenesis of human autoimmune diseases. Our observations on the defects of seven PKC isoenzymes in the peripheral blood mononuclear cells (PBMC) demonstrate that these molecular impairments are not prerequisits of the pathogenesis of systemic lupus erythematosus (SLE), mixed connective tissue disease and Sjögren's syndrome. However, these defects can modulate the disease activity and symptoms especially in SLE by several pathways. The role of PKC system in other forms of autoimmune diseases is also very small. It was of note that we detected decreased expression of PKC isoenzymes in PBMC of a European white family with an X-linked genetic background showing seasonal undulations in the lupus patient and also in her healthy mother.
•The physiological role of protein kinase C (PKC) enzymes in the immune system.•Collection of earlier data on the defects of PKC isoenzymes (one-two enzymes) in the pathogenesis of human autoimmune diseases. (The results of others)•Data on 7 PKC isoenzymes of mononuclear cells in systemic lupus erythematosus mixed connective tissue disease and Sjögren's syndrome.•P athways of defected PKC isoenzymes modifying the disease activity and symptoms in SLE without being prerequisites for the pathogenesis of SLE. |
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Bibliography: | ObjectType-Article-2 SourceType-Scholarly Journals-1 ObjectType-Feature-3 content type line 23 ObjectType-Review-1 |
ISSN: | 1521-6616 1521-7035 |
DOI: | 10.1016/j.clim.2022.109071 |