Document Type : Mini-reviews
Authors
1
Department of Microbiology and Immunology, Faculty of pharmacy, University of Sadat City, Egypt
2
Department of Microbiology and Immunology, Faculty of Pharmacy, Suez Canal University, Ismailia, Egypt
3
Department of Histology and Cell Biology (Genetics Unit), Faculty of Medicine, Suez Canal University, 41522, Ismailia, Egypt; Center of Excellence in Molecular and Cellular Medicine, Faculty of Medicine, Suez Canal University, 41522, Ismailia, Egypt.
4
Department of Anesthesia and Intensive care, Faculty of Medicine, Suez Canal University, Ismailia, Egypt.
5
Department of Microbiology and Immunology, Faculty of Pharmacy, Fayoum University, Fayoum, Egypt
6
Department of Microbiology and Immunology, Faculty of Pharmacy, Suez Canal university, Ismailia, 41522, Egypt;
Abstract
Complement system has a very important role in our defense against different pathogens and harmful immune complexes. The lectin pathway of complement system is activated by mannose binding lectin leading to complement cascade ending with the removal of these invading pathogens and the injuring immune complexes. Defects in mannose binding lectin were found to be associated with MBL2 gene polymorphisms such as exon 1 polymorphisms and promotor region polymorphisms. These defects were linked to serious autoimmune diseases such as systemic lupus erythematosus and rheumatoid arthritis. The aim of our review is to provide an overview of mannose binding lectin role in complement system and to outline the information about mannose binding lectin defects with systemic lupus erythematosus and rheumatoid arthritis in addition to the possible related explanations. Mannose binding lectin variants were believed to have an association with these autoimmune disorders by many studies with the presence of conflicted studies as well.
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