New Pathogenic Mechanisms in Autoimmune Diseases: Focus on Immune-Regulatory Pathways

A special issue of Cells (ISSN 2073-4409). This special issue belongs to the section "Cellular Pathology".

Deadline for manuscript submissions: closed (30 September 2023) | Viewed by 1910

Special Issue Editors


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Guest Editor
Rheumatology Unit, Dipartimento di Scienze Cliniche Internistiche, Anestesiologiche e Cardiovascolari, Sapienza University of Rome, Rome, Italy
Interests: systemic lupus erythematosus; rheumatoid arthritis; Sjogren syndrome; antiphospholipid syndrome; arthritis induced by immune checkpoint inhibitors
Special Issues, Collections and Topics in MDPI journals

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Guest Editor
Lupus Clinic, Reumatologia, Dipartimento di Scienze Cliniche Internistiche Anestesiologiche e Cardiovascolari, Sapienza Università di Roma, Rome, Italy
Interests: autoimmune diseases; systemic lupus erythematosus; genetic factors; pathogenic mechanisms; biomarkers

E-Mail Website
Guest Editor
Lupus Clinic, Reumatologia, Dipartimento di Scienze Cliniche Internistiche Anestesiologiche e Cardiovascolari, Sapienza Università di Roma, Rome, Italy
Interests: autoimmune diseases; systemic lupus erythematosus; genetic factors; pathogenic mechanisms; biomarkers
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

It is with great pleasure and enthusiasm that we present this Special Issue of Cells, entitled “New Pathogenic Mechanisms in Autoimmune Diseases: Focus on Immune-Regulatory Pathways”.

This issue will investigate the recent pathogenic aspects underlining autoimmune diseases in order to unveil the complexity of these conditions, especially systemic lupus erythematosus.

The spread of drugs that target immune checkpoints in cancer treatment has refocused immunology regarding the possible role of co-stimulatory molecules in the pathogenesis of autoimmune diseases.

In this field, some pathways have been clearly defined, leading to the development of Abatacept (CTLA4–Ig), a fusion protein designed to modulate the T cell co-stimulatory signal mediated through the CD28–CD80/86 pathway. Indeed, several studies demonstrated the efficacy and safety of this biological drug in rheumatoid arthritis.

Furthermore, other promising mechanisms have been investigated, including other co-stimulatory molecules and immune-regulatory cells.  

This Special Issue aims to present new, exploratory research concerning immune-regulatory pathways in systemic autoimmune diseases, considering the following conditions:

  1. Systemic Lupus Erythematosus;
  2. Inflammatory arthropathies;
  3. Sjögren Syndrome;
  4. Systemic Sclerosis;
  5. Myositis and Vasculitis;
  6. Immune-related adverse events associated with treatment with immune-checkpoints inhibitors.

We look forward to receiving your contributions summarizing or explaining your research for this Special Issue.

Dr. Fulvia Ceccarelli
Dr. Francesco Natalucci
Dr. Giulio Olivieri
Guest Editors

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Keywords

  • autoimmune diseases 
  • pathogenesis 
  • cells 
  • immune regulatory mechanisms 
  • co-stimulatory molecules

Published Papers (1 paper)

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Research

10 pages, 2072 KiB  
Communication
Involvement of Substance P (SP) and Its Related NK1 Receptor in Primary Sjögren’s Syndrome (pSS) Pathogenesis
by Pamela Rosso, Elena Fico, Serena Colafrancesco, Mario Giuseppe Bellizzi, Roberta Priori, Bruna Cerbelli, Martina Leopizzi, Carla Giordano, Antonio Greco, Paola Tirassa, Cinzia Severini and Massimo Fusconi
Cells 2023, 12(10), 1347; https://doi.org/10.3390/cells12101347 - 9 May 2023
Cited by 1 | Viewed by 1565
Abstract
Primary Sjögren’s Syndrome (pSS) is a systemic autoimmune disease that primarily attacks the lacrimal and salivary glands, resulting in impaired secretory function characterized by xerostomia and xerophthalmia. Patients with pSS have been shown to have impaired salivary gland innervation and altered circulating levels [...] Read more.
Primary Sjögren’s Syndrome (pSS) is a systemic autoimmune disease that primarily attacks the lacrimal and salivary glands, resulting in impaired secretory function characterized by xerostomia and xerophthalmia. Patients with pSS have been shown to have impaired salivary gland innervation and altered circulating levels of neuropeptides thought to be a cause of decreased salivation, including substance P (SP). Using Western blot analysis and immunofluorescence studies, we examined the expression levels of SP and its preferred G protein-coupled TK Receptor 1 (NK1R) and apoptosis markers in biopsies of the minor salivary gland (MSG) from pSS patients compared with patients with idiopathic sicca syndrome. We confirmed a quantitative decrease in the amount of SP in the MSG of pSS patients and demonstrated a significant increase in NK1R levels compared with sicca subjects, indicating the involvement of SP fibers and NK1R in the impaired salivary secretion observed in pSS patients. Moreover, the increase in apoptosis (PARP-1 cleavage) in pSS patients was shown to be related to JNK phosphorylation. Since there is no satisfactory therapy for the treatment of secretory hypofunction in pSS patients, the SP pathway may be a new potential diagnostic tool or therapeutic target. Full article
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