Violeta
Senior Member
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R. M. Dommett, 1 N Klein, 1 and M. W. Turner
2
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7169806/
MBL disease association studies have been a fruitful area of research and implicate a role for MBL in infective, inflammatory and autoimmune disease processes.
Our understanding of MBL function has grown rapidly over the past three decades. It is now recognized to have a role in processes as diverse as complement activation, promotion of complement‐independent opsonophagocytosis, modulation of inflammation, recognition of altered self‐structures and apoptotic cell clearance.
Nevertheless, a recent meta‐analysis has reviewed studies in this area and found that MBL variant alleles are indeed SLE risk factors. As with infectious disease, there is some evidence that the risk of pathology increases if there is another co‐existing immune defect. For example, in a cohort of Spanish patients, the odds ratio for developing SLE was 2.4 for individuals with MBL deficiency, but this increased to 3.2 when there was also a co‐existing partial C4 deficiency.
Studies in patients with SLE have reported that MBL deficiency also influences their risk of developing certain complications, which include arterial thromboses and respiratory tract infections.
A role for MBL in the pathogenesis of rheumatoid arthritis has also been suggested. Malhotra et al. reported that changes in IgG glycosylation secondary to the underlying disease results in MBL‐associated complement activation. Such complement activation then contributes to chronic inflammation of the synovial membrane.
However, Graudal et al. found that patients with lower MBL levels experienced earlier, more severe, symptoms and had more rapid joint destruction as visualized radiologically.
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7169806/
MBL disease association studies have been a fruitful area of research and implicate a role for MBL in infective, inflammatory and autoimmune disease processes.
Our understanding of MBL function has grown rapidly over the past three decades. It is now recognized to have a role in processes as diverse as complement activation, promotion of complement‐independent opsonophagocytosis, modulation of inflammation, recognition of altered self‐structures and apoptotic cell clearance.
MBL and autoimmune disease
As a component of the complement system with similarities to C1q, but also as a player in infectious and inflammatory processes, the structure and function of MBL have prompted studies exploring a possible role in autoimmune conditions. Systemic lupus erythematosus (SLE) has been the focus of a number of MBL genotyping studies, but the results have been somewhat inconsistent.Nevertheless, a recent meta‐analysis has reviewed studies in this area and found that MBL variant alleles are indeed SLE risk factors. As with infectious disease, there is some evidence that the risk of pathology increases if there is another co‐existing immune defect. For example, in a cohort of Spanish patients, the odds ratio for developing SLE was 2.4 for individuals with MBL deficiency, but this increased to 3.2 when there was also a co‐existing partial C4 deficiency.
Studies in patients with SLE have reported that MBL deficiency also influences their risk of developing certain complications, which include arterial thromboses and respiratory tract infections.
A role for MBL in the pathogenesis of rheumatoid arthritis has also been suggested. Malhotra et al. reported that changes in IgG glycosylation secondary to the underlying disease results in MBL‐associated complement activation. Such complement activation then contributes to chronic inflammation of the synovial membrane.
However, Graudal et al. found that patients with lower MBL levels experienced earlier, more severe, symptoms and had more rapid joint destruction as visualized radiologically.