Search for Articles:
Title / Keyword
Author / Affiliation / Email
Journal
Article Type
 
 
Advanced Search
 
Section
Special Issue
Volume
Issue
Number
Page
 
8.1
4.9
Journals
IJMS
Special Issues
Innate Immunity in Autoimmune Diseases
ijms-logo
Submit to Special Issue Submit Abstract to Special Issue Review for IJMS Propose a Special Issue

Journal Menu

► Journal Menu

Journal Browser

► Journal Browser
share announcement

Innate Immunity in Autoimmune Diseases

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: 31 August 2024 | Viewed by 913

Special Issue Editors

Prof. Dr. Francesca Wanda Rossi

E-Mail Website
Guest Editor
Department of Translational Medical Sciences (DiSMeT), Center for Basic and Clinical Immunology Research (CISI), WAO Center of Excellence, University of Naples Federico II, 80131 Naples, Italy
Interests: immunology; autoimmune diseases, allergic and inflammatory diseases; biological therapies; basophils; mast cells; fibroblasts; uPAR/uPAR system and its involvement in inflammation; VEGF and its receptors; FPRs receptors; tissue repair processes and tissue remodeling
Special Issues, Collections and Topics in MDPI journals
Dr. Maria Rosaria Galdiero

E-Mail Website
Guest Editor
Department of Translational Medical Sciences (DiSMeT), Center for Basic and Clinical Immunology Research (CISI), WAO Center of Excellence, University of Naples Federico II, 80131 Naples, Italy
Interests: immunology; autoimmunity; biological therapies; immune checkpoint inhibitors; immune-related adverse events; autoimmune diseases; neutrophils; macrophages; mast cells; cancer-related inflammation; cancer immunology; tissue repair processes and tissue remodeling
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues, 

The innate immune system comprises a variety of factors that influence and participate in virtually all aspects of inflammation and immunity. It is crucial for host defense, but under special conditions, the activation of cells of the innate immune system can break the state of inactivity in auto-reactive cells of the adaptive immune system, thereby provoking autoimmune diseases, such as rheumatoid arthritis (RA), systemic lupus erythematosus (SLE), multiple sclerosis (MS) or inflammatory bowel disease. Multiple steps and multiple components of both the innate and the adaptive immune system are implicated in the generation of autoimmunity and therefore diseases. The innate immune system is crucial to both the beginning and end of autoimmunity. This Special Issue aims to open a discussion on these themes through valuable contributions from pathologists, rheumatologists, dermatologists, and gastroenterologists, creating a common forum for exchanging information and presenting the most cutting edge knowledge in the field. Since IJMS is a journal of molecular science, we will first accept original articles and then outstanding reviews. Clinical submissions with biomolecular experiments and model submissions with at least some validated data (or biological experiments) are also welcomed. Models or clinical studies will not be suitable for our journal, and case reports are not recommended.

Prof. Dr. Francesca Wanda Rossi
Dr. Maria Rosaria Galdiero
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 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

  • autoimmune diseases
  • basophils
  • neutrophils
  • eosinophils
  • macrophages
  • mast cells
  • innate receptors
  • TLRs
  • FPRs
  • uPAR/uPA
  • T cells
  • B cells
  • NETs
  • biomarkers
  • biological therapies
  • cytokines

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

12 pages, 1895 KiB  
Article
Toll-like Receptor Homologue CD180 Ligation of B Cells Upregulates Type I IFN Signature in Diffuse Cutaneous Systemic Sclerosis
by Szabina Erdő-Bonyár, Judit Rapp, Rovéna Subicz, Kristóf Filipánits, Tünde Minier, Gábor Kumánovics, László Czirják, Tímea Berki and Diána Simon
Int. J. Mol. Sci. 2024, 25(14), 7933; https://doi.org/10.3390/ijms25147933 (registering DOI) - 20 Jul 2024
Viewed by 311
Abstract
Type I interferon (IFN-I) signaling has been shown to be upregulated in systemic sclerosis (SSc). Dysregulated B-cell functions, including antigen presentation, as well as antibody and cytokine production, all of which may be affected by IFN-I signaling, play an important role in the [...] Read more.
Type I interferon (IFN-I) signaling has been shown to be upregulated in systemic sclerosis (SSc). Dysregulated B-cell functions, including antigen presentation, as well as antibody and cytokine production, all of which may be affected by IFN-I signaling, play an important role in the pathogenesis of the disease. We investigated the IFN-I signature in 71 patients with the more severe form of the disease, diffuse cutaneous SSc (dcSSc), and 33 healthy controls (HCs). Activation via Toll-like receptors (TLRs) can influence the IFN-I signaling cascade; thus, we analyzed the effects of the TLR homologue CD180 ligation on the IFN-I signature in B cells. CD180 stimulation augmented the phosphorylation of signal transducer and activator of transcription 1 (STAT1) in dcSSc B cells (p = 0.0123). The expression of IFN-I receptor (IFNAR1) in non-switched memory B cells producing natural autoantibodies was elevated in dcSSc (p = 0.0109), which was enhanced following anti-CD180 antibody treatment (p = 0.0125). Autoantibodies to IFN-Is (IFN-alpha and omega) correlated (dcSSc p = 0.0003, HC p = 0.0192) and were present at similar levels in B cells from dcSSc and HC, suggesting their regulatory role as natural autoantibodies. It can be concluded that factors other than IFN-alpha may contribute to the elevated IFN-I signature of dcSSc B cells, and one possible candidate is B-cell activation via CD180. Full article
(This article belongs to the Special Issue Innate Immunity in Autoimmune Diseases)
►▼ 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