Complement in autoimmune diseases

Vignesh, Pandiarajan; Rawat, Amit; Sharma, Manisha; Singh, Surjit

doi:10.1016/j.cca.2016.12.017

Cited by 99 publications

(65 citation statements)

References 116 publications

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“…This clearly points toward the differential expression of these two antagonistic complement regulators during the development of human B-cells, a phenomenon which may influence the maintenance of peripheral B-cell tolerance. Deficiencies in upstream complement molecules, including C1q, C2, and C4, may result in inefficient clearance, in the absence of which these products become a source of autoantigens for B-cells and a probable source of an autoimmune response ( 137 ). In addition to complement receptors, attachment of C4b to self-antigen and localization of these complexes to CD35 on stromal cells within the bone marrow also regulate the selection of potentially autoreactive B-cells ( 138 ).…”

Section: Complement and Adaptive Immunitymentioning

confidence: 99%

Complement After Trauma: Suturing Innate and Adaptive Immunity

2018

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The overpowering effect of trauma on the immune system is undisputed. Severe trauma is characterized by systemic cytokine generation, activation and dysregulation of systemic inflammatory response complementopathy and coagulopathy, has been immensely instrumental in understanding the underlying mechanisms of the innate immune system during systemic inflammation. The compartmentalized functions of the innate and adaptive immune systems are being gradually recognized as an overlapping, interactive and dynamic system of responsive elements. Nonetheless the current knowledge of the complement cascade and its interaction with adaptive immune response mediators and cells, including T- and B-cells, is limited. In this review, we discuss what is known about the bridging effects of the complement system on the adaptive immune system and which unexplored areas could be crucial in understanding how the complement and adaptive immune systems interact following trauma.

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Section: Complement and Adaptive Immunitymentioning

confidence: 99%

Complement After Trauma: Suturing Innate and Adaptive Immunity

2018

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“…The lectin pathway, along with both classical and alternative pathways intersects at the cleavage of C3 and C5 followed by the opsonization of C3b and pathogen phagocytosis or eradication of pathogen by the arrangement of a membrane attack complex (MAC) [17].…”

Section: Introductionmentioning

confidence: 99%

The Clinical Value of Ficolin-3 Gene Polymorphism in Rheumatic Heart Disease. An Egyptian Adolescents Study

Gomaa

Khidr

Elshafei

et al. 2020

Preprint

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Background: The innate immunity molecules against Streptococcus pyogenes infections include ficolin-3 that was thought to have a role in autoimmune diseases resulting from this infection such as rheumatic fever (RF) which goes on and leads to its most serious sequel, rheumatic heart disease (RHD). We aimed in this study to disclose if there is an association between ficolin-3 gene polymorphisms (rs4494157 and rs10794501) and RF with or without RHD for the first time in Egyptian adolescents. Methods: This study was carried out on 160 RF patients; eighty patients had RHD and eighty didn't have RHD. Besides, eighty ethnically and age-matched healthy subjects were selected as control. Ficolin-3 gene polymorphisms (rs4494157 and rs10794501) were genotyped by TaqMan® allelic discrimination assay. Serum ficolin-3 was quantitatively determined by ELISA. Results: Regarding ficolin-3 gene polymorphisms; no differences in the frequency of rs10794501 were found between the investigated groups, while polymorphism of rs4494157 showed a significant correlation between AA homozygous genotype, high serum ficolin-3, and RHD risk. Conclusion: Elevated serum ficolin-3 and carriage of AA genotype of rs4494157 appeared to be involved in RF and RHD pathogenesis and may be predictive tools for early recognition of RHD prone RF patients, and subsequent early prophylactic interventions.

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“…Binding to these receptors, BLyS can inhibit apoptosis and contribute to the proliferation and differentiation of B lymphocytes into Ig‐producing plasma cells in MG . Preventing BLyS from binding its receptors is a potential approach to interrupting BLyS‐induced B lymphocyte proliferation and differentiation in MG …”

Section: Potential Targets Of Mabs and Their Applicationmentioning

confidence: 99%

Myasthenia gravis and specific immunotherapy: monoclonal antibodies

Cai

et al. 2019

Annals of the New York Academy of Sciences

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Myasthenia gravis (MG) is an acquired autoimmune disease affecting the postsynaptic membrane of neuromuscular junctions and characterized by antibody-mediated T cell dependence and complement involvement. Cholinesterase inhibitors (e.g., pyridostigmine bromide), glucocorticoids, and azathioprine are currently recommended as firstline treatments for MG, though they have limitations, including potential toxicity and ineffectiveness in patients with refractory MG. In recent years, owing to an increasing understanding of MG pathogenesis the development and execution of clinical trials with novel biologics, including monoclonal antibodies (mAbs) that have demonstrated higher safety and more specificity, provide new opportunities for the treatment of MG. In this article, we review recent advances in MG pathogenesis and the mAbs that have been used for target-specific MG therapy.

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Complement in autoimmune diseases

Cited by 99 publications

References 116 publications

Complement After Trauma: Suturing Innate and Adaptive Immunity

Complement After Trauma: Suturing Innate and Adaptive Immunity

The Clinical Value of Ficolin-3 Gene Polymorphism in Rheumatic Heart Disease. An Egyptian Adolescents Study

Myasthenia gravis and specific immunotherapy: monoclonal antibodies

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