Special Issue "Complement System in Disease"

A special issue of Biomolecules (ISSN 2218-273X). This special issue belongs to the section "Molecular Medicine".

Deadline for manuscript submissions: closed (10 September 2021).

Special Issue Editors

Prof. Jean van den Elsen
E-Mail Website
Guest Editor
Department of Biology & Biochemistry, University of Bath, Bath, UK
Interests: immunology; complement system; structural biology
Dr. Maisem Laabei
E-Mail Website
Guest Editor
Department of Biology & Biochemistry, University of Bath, Bath, UK
Interests: immune evasion; bacterial pathogenesis; complement system; Staphylococcus aureus

Special Issue Information

Dear Colleagues,

The complement system is an essential innate immune pathway that exhibits extensive immunomodulatory functions through close communication with multiple biological systems. At its core, the rapid activation and amplification of complement directs the elimination of pathogens.

Although complement primarily evolved as a host defence system, increasing evidence indicates broader roles in immune surveillance and homeostasis. Recent studies illustrate the role of complement in coordinating inflammatory processes, assisting the recycling and elimination of dying cells and immune complexes, instructing and modulating adaptive immunity, regulating cellular metabolic processes and shaping neural development.

The dysregulation of complement tips the balance from protection to destruction. Complement disruption drives a number of immune, inflammatory and degenerative diseases, either playing a prominent role such as in paroxysmal nocturnal haemoglobinuria (PNH) or contributing to disease via the promotion of exaggerated inflammatory and immune responses. The list of disorders associated with complement is growing, incentivising the development of therapeutics to control complement activity. Complement therapies have shown promise in treating a multitude of pathologies, including alleviating inflammatory lung complications in COVID-19 patients.

This Special Issue will focus on a variety of aspects related to Complement in Human Disease. Original research manuscripts and reviews dealing with the topics outlined are very welcome.

Prof. Jean van den Elsen
Dr. Maisem Laabei
Guest Editors

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All papers will be peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. Biomolecules is an international peer-reviewed open access monthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2100 CHF (Swiss Francs). Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

  • Molecular mechanisms underpinning complement-related diseases
  • Structural basis of complement function/activity
  • Complement and cellular metabolism
  • Microbial complement evasion mechanisms
  • New developments in complement in health and disease
  • Therapeutic targeting of complement
  • Complement in COVID-19.

Published Papers (2 papers)

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Research

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Article
Soluble Complement Component 1q Receptor 1 (sCD93) Is Associated with Graft Function in Kidney Transplant Recipients
Biomolecules 2021, 11(11), 1623; https://doi.org/10.3390/biom11111623 - 02 Nov 2021
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Abstract
Cluster of differentiation 93 (CD93), also known as complement component 1q receptor 1 is a transmembrane glycoprotein expressed in endothelial and hematopoietic cells and associated with phagocytosis, cell adhesion, angiogenesis and inflammation. The extracellular part, soluble CD93 (sCD93), is released to body fluids [...] Read more.
Cluster of differentiation 93 (CD93), also known as complement component 1q receptor 1 is a transmembrane glycoprotein expressed in endothelial and hematopoietic cells and associated with phagocytosis, cell adhesion, angiogenesis and inflammation. The extracellular part, soluble CD93 (sCD93), is released to body fluids in inflammation. Data on sCD93 in kidney diseases are limited. Our aim was to evaluate serum sCD93 in long-term kidney transplant recipients as a marker of inflammation and endothelial dysfunction that may be potentially useful in early recognition of graft dysfunction. Seventy-eight adult patients with functioning kidney graft and stable clinical state were examined at least one year after kidney transplantation. Serum sCD93 was measured by enzyme immunosorbent assay. Estimated glomerular filtration rate (eGFR) and albuminuria or proteinuria were assessed at baseline and over one-year follow-up. Increased sCD93 was associated with lower baseline eGFR independently of the confounders. Moreover, sCD93 was negatively associated with eGFR during one-year follow-up in simple analysis; however, this was not confirmed after adjustment for confounders. Baseline sCD93 was positively associated with baseline albuminuria and with increased proteinuria during the follow-up. Serum sCD93 was not correlated with other studied inflammatory markers (interleukin 6, C-reactive protein, procalcitonin and C3 and C4 complement components). To the best of our knowledge, this is the first report regarding the concentrations of sCD93 in kidney transplant recipients and one of the first reports showing the inverse association between sCD93 and renal function. Serum sCD93 should be further evaluated as a diagnostic and prognostic marker in renal transplantation. Full article
(This article belongs to the Special Issue Complement System in Disease)
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Review

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Review
Complement Components in the Diagnosis and Treatment after Kidney Transplantation—Is There a Missing Link?
Biomolecules 2021, 11(6), 773; https://doi.org/10.3390/biom11060773 - 21 May 2021
Cited by 1 | Viewed by 730
Abstract
Currently, kidney transplantation is widely accepted as the renal replacement therapy allowing for the best quality of life and longest survival of patients developing end-stage renal disease. However, chronic transplant rejection, recurrence of previous kidney disease or newly acquired conditions, or immunosuppressive drug [...] Read more.
Currently, kidney transplantation is widely accepted as the renal replacement therapy allowing for the best quality of life and longest survival of patients developing end-stage renal disease. However, chronic transplant rejection, recurrence of previous kidney disease or newly acquired conditions, or immunosuppressive drug toxicity often lead to a deterioration of kidney allograft function over time. Complement components play an important role in the pathogenesis of kidney allograft impairment. Most studies on the role of complement in kidney graft function focus on humoral rejection; however, complement has also been associated with cell mediated rejection, post-transplant thrombotic microangiopathy, the recurrence of several glomerulopathies in the transplanted kidney, and transplant tolerance. Better understanding of the complement involvement in the transplanted kidney damage has led to the development of novel therapies that inhibit complement components and improve graft survival. The analysis of functional complotypes, based on the genotype of both graft recipient and donor, may become a valuable tool for assessing the risk of acute transplant rejection. The review summarizes current knowledge on the pathomechanisms of complement activation following kidney transplantation and the resulting diagnostic and therapeutic possibilities. Full article
(This article belongs to the Special Issue Complement System in Disease)
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