Emerging Molecular Targets in Sjogren’s Syndrome 2.0

Dear Colleagues,

Sjogren’s syndrome (SjS) is an autoimmune inflammatory lymphoproliferative disease, in which genetic and environmental factors play a fundamental role, causing the dysfunction of T cells, B cells, and the production of autoantibodies. The inflammatory process in SjS affects exocrine glands, particularly salivary glands. Genome-wide association studies have identified numerous loci that may harbor susceptibility genes, although the functional significance of most of these polymorphisms remains currently unknown. In addition to the impact of the human leukocyte antigen locus, the best-characterized genes codify for molecules involved in different immunological pathways, including the signal transducer and activator of transcription 4, mainly implicated in Th17 activation and differentiation, and the interferon regulatory factor, which is involved in type 1 interferon signaling. Endogenous retroviruses have long been implicated in triggering autoimmunity through structural and functional molecular mimicry with viral proteins. Autoantibodies are a hallmark of the disease and may depict specific clinical phenotypes. Current therapies largely rely on the use of corticosteroids and immunosuppressants. Interference with pro-inflammatory cytokines and mechanisms that link innate and adaptive immunity offers new options in the treatment of SjS. Several intriguing approaches, for instance, those directed against Toll-like receptors, inflammasome chemokines or those that target the inhibition of apoptosis, have emerged and are directed at preserving and restoring functional exocrine tissue. A rational approach for therapeutic design requires a detailed understanding of disease pathogenesis, and the chance to use biological and targeted synthetic DMARDs represents an emerging new era for patients with SjS.

Potential topics include, but are not limited to, the following:

• The role of genetics in the pathogenesis of SjS;
• Biomarkers and SjS;
• T cells in SjS;
• Autoantibodies in SjS;
• Novel potential compounds in SjS;
• Emerging new strategies for the treatment of patients with SjS.

Papers are published upon acceptance, regardless of the Special Issue publication date.

The deadline for submission is 30 June 2023.

Regarding formatting, reviews, original articles, and brief articles are acceptable.

There are no restrictions in the length of manuscripts, but the text should be concise and comprehensive. If possible, the abstract should be limited to 250 words, and we ask you to provide 3–10 keywords for future indexing purposes. Review papers should contain at least 3500 words of text in the main body. References should be up-to-date. We suggest including at least one summative table or figure in the manuscript.

Dr. Elena Bartoloni
Prof. Dr. Roberto Gerli 
Dr. Carlo Perricone
Guest Editors

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