Search for Articles:
Title / Keyword
Author / Affiliation / Email
Journal
Article Type
 
 
Advanced Search
 
Section
Special Issue
Volume
Issue
Number
Page
 
9.0
4.9
Journals
IJMS
Special Issues
Autoimmune Diseases: From Molecular Basis to Therapy
ijms-logo
Submit to IJMS Review for IJMS Propose a Special Issue

Journal Menu

► Journal Menu

Journal Browser

► Journal Browser
share announcement

Autoimmune Diseases: From Molecular Basis to Therapy

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Immunology".

Deadline for manuscript submissions: closed (31 January 2025) | Viewed by 1498

Special Issue Editor

Dr. Raquel López-Mejías

E-Mail Website
Guest Editor
Valdecilla Research Institute (IDIVAL), 39008 Santander, Spain
Interests: vasculitis; IgAV; nephritis; genetics; molecular; autoimmune diseases
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Autoimmune diseases are a group of pathologies characterized by an abnormal immune response and inflammatory and tissue damage. Clinical differences have been described among them, although common molecular mechanisms underlie them. Interestingly, the specific molecular mechanisms are still unknown. In this regard, identification of the molecular mechanisms (at genetic, epigenetic, molecular, and cellular levels) is an issue of great interest. This will help to establish an early and accurate diagnosis, identify the molecular mechanisms driving the autoimmune disease, prevent the development of the comorbidities associated with them, and develop therapeutic strategies more specific for the treatment of these conditions. In this Special Issue, we welcome authors to submit original research and review articles contributing to the understanding of this area, which include, but are not limited to, the following topics: the role of genetics in autoimmune diseases; the role of epigenetics in autoimmune diseases; molecules and cells implicated in autoimmune diseases; and molecular mechanisms implicated in the development of autoimmune diseases and their comorbidities.

This Special Issue is Led by Dr. Raquel López-Mejías and assisted by our Topical Advisory Panel Member Dr. Ilaria Mormile (Department of Translational Medical Sciences, University of Naples Federico II, Naples, Italy). We welcome your submission!

Dr. Raquel López-Mejías
Guest Editor

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 submissions that pass pre-check are 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. International Journal of Molecular Sciences is an international peer-reviewed open access semimonthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. There is an Article Processing Charge (APC) for publication in this open access journal. For details about the APC please see here. 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

  • genetics
  • epigenetics
  • molecules
  • autoimmune diseases
  • inflammation
  • cell-mediated immunity

Benefits of Publishing in a Special Issue

  • Ease of navigation: Grouping papers by topic helps scholars navigate broad scope journals more efficiently.
  • Greater discoverability: Special Issues support the reach and impact of scientific research. Articles in Special Issues are more discoverable and cited more frequently.
  • Expansion of research network: Special Issues facilitate connections among authors, fostering scientific collaborations.
  • External promotion: Articles in Special Issues are often promoted through the journal's social media, increasing their visibility.
  • Reprint: MDPI Books provides the opportunity to republish successful Special Issues in book format, both online and in print.

Further information on MDPI's Special Issue policies can be found here.

Published Papers (1 paper)

Order results
Result details
Show export options expand_more Show export options expand_less
Select all
Export citation of selected articles as:

Research

17 pages, 2636 KiB  
Article
Development of Peptide Mimics of the Human Acetylcholine Receptor Main Immunogenic Region for Treating Myasthenia Gravis
by Vu B. Trinh and Robert H. Fairclough
Int. J. Mol. Sci. 2025, 26(1), 229; https://doi.org/10.3390/ijms26010229 - 30 Dec 2024
Cited by 1 | Viewed by 885
Abstract
We have designed and produced 39 amino acid peptide mimics of the Torpedo and human acetylcholine receptors’ (AChRs) main immunogenic regions (MIRs). These conformationally sensitive regions consist of three non-contiguous segments of the AChR α-subunits and are the target of 50–70% of the [...] Read more.
We have designed and produced 39 amino acid peptide mimics of the Torpedo and human acetylcholine receptors’ (AChRs) main immunogenic regions (MIRs). These conformationally sensitive regions consist of three non-contiguous segments of the AChR α-subunits and are the target of 50–70% of the anti-AChR autoantibodies (Abs) in human myasthenic serum and in the serum of rats with a model of that disease, experimental autoimmune myasthenia gravis (EAMG), induced by immunizing the rats with the Torpedo electric organ AChR. These MIR segments covalently joined together bind a significant fraction of the monoclonal antibodies (mAbs) raised in rats against electric organ AChR. Many of these mAbs cross react with the rat neuromuscular AChR MIR and induce myasthenic symptoms when injected into naïve rats. The human MIR mimic peptide (H39MIR) is evolutionarily related to that of the Torpedo electric organ MIR mimic peptide (T39MIR) with eight amino acid differences between the two MIR mimics. The mAbs raised to the electric organ AChR MIR cross react with the human and scores of other species’ neuromuscular AChRs. However, the mAbs do not cross react with the H39MIR mimic attached to the N-terminus of an intein–chitin-binding domain (H39MIR-IChBD) even though they do bind to the T39MIR-IChBD construct. To account for this difference in binding anti-MIR mAbs, each of the eight human amino acids was substituted individually into the T39MIR-IChBD, and four of them were found to weaken mAb recognition. Substituting the corresponding four Torpedo amino acids individually and in combination into the homologous positions in H39MIR-IChBD makes chimeric human MIR mimic peptides (T/H39MIR), some of which bind anti-MIR mAbs and anti-MIR Abs from rat EAMG and human MG sera. The best mAb binding chimeric peptide constructs may potentially serve as the basis of a diagnostic anti-MIR Ab titer assay that is both prognostic and predictive of disease severity. Furthermore, the best peptides may also serve as the targeting element of a non-steroidal antigen-specific treatment of MG to remove anti-AChR MIR Abs, either as fused to the N-terminals of the human immunoglobin Fc fragment or as the targeting component of a T cell chimeric autoantibody receptor (CAAR) directed to anti-MIR memory B cells for elimination. Full article
(This article belongs to the Special Issue Autoimmune Diseases: From Molecular Basis to Therapy)
►▼ Show Figures

Figure 1

Show export options expand_more Show export options expand_less
Select all
Export citation of selected articles as:
 
Displaying articles 1-1
Back to TopTop