Background: Oral lichen planus (OLP) is a T cell-mediated chronic autoimmune disease, whose pathogenesis and etiology are not entirely understood. OLP is characterized by subepithelial lymphocyte infiltration and elevated intra-epithelial lymphocytes. The majority of lamina propria lymphocytes are CD4 T cells. CD4 helper T (Th) cells play a crucial role in activating CD8 cytotoxic T cells (CTLs) through interactions and cytokine production. Th1 and Th2 cells are well-accepted to be associated with OLP pathogenesis. However, OLP treatment is challenging yet, the more information we have about the pathology of OLP, the easier it will be treated. With the discovery of Th17 cells in recent years and the demonstration of their role in autoimmune disease, many researchers started to investigate the role of Th17 in the pathogenesis of OLP.

Methods: To make up this review, studies covering the role of TH17 in different types of lichen planus were selected from major databases.

Results: As we review in this article, Th17 cells and their signature cytokines play an important role in OLP pathogenesis. As well, utilizing some anti-IL-17 antibodies showed promising results in improving the disease; however, more studies are still needed to better understand and treat OLP.

Download full-text PDF

Source
http://dx.doi.org/10.1007/s00011-023-01763-7DOI Listing

Publication Analysis

Top Keywords

th17 cells
12
lichen planus
12
oral lichen
8
autoimmune disease
8
olp pathogenesis
8
role th17
8
cells
7
olp
7
th17
5
pathogenesis
5

Similar Publications

Plague, caused by , poses a public health threat not only due to sporadic outbreaks across the globe but also due to its potential as a biothreat agent. Ironically, among the seven deadliest pandemics in global history, three were caused by . Pneumonic plague, the more contagious and severe form of the disease, is difficult to contain, requiring either prophylactic antibiotic treatment or vaccination.

View Article and Find Full Text PDF

Oral Delivery of miR146a Conjugated to Cerium Oxide Nanoparticles Improves an Established T Cell-Mediated Experimental Colitis in Mice.

Pharmaceutics

December 2024

Laboratory for Fetal and Regenerative Biology, Department of Surgery, University of Arizona Tucson College of Medicine, Banner Children's at Diamond Children's Medical Center, 1656 E Mabel St, Rm 230, Tucson, AZ 85721, USA.

Dysregulated inflammation and oxidative stress are strongly implicated in the pathogenesis of inflammatory bowel disease. We have developed a novel therapeutic that targets inflammation and oxidative stress. It is comprised of microRNA-146a (miR146a)-loaded cerium oxide nanoparticles (CNPs) (CNP-miR146a).

View Article and Find Full Text PDF

Targeted Therapy for Severe Sjogren's Syndrome: A Focus on Mesenchymal Stem Cells.

Int J Mol Sci

December 2024

Departments of Genetics, Microbiology and Immunology, Center for Research on Harmful Effects of Biological and Chemical Hazards, Faculty of Medical Sciences, University of Kragujevac, 69 Svetozara Markovica Street, 34000 Kragujevac, Serbia.

Primary Sjögren's syndrome (pSS) is an autoimmune disease characterized by the infiltration of lymphocytes on salivary and lacrimal glands, resulting in their dysfunction. Patients suffering from severe pSS have an increased risk of developing multi-organ dysfunction syndrome due to the development of systemic inflammatory response, which results in immune cell-driven injury of the lungs, kidneys, liver, and brain. Therapeutic agents that are used for the treatment of severe pSS encounter various limitations and challenges that can impact their effectiveness.

View Article and Find Full Text PDF

Blocking the Sphingosine-1-Phosphate Receptor 2 (S1P) Reduces the Severity of Collagen-Induced Arthritis in DBA-1J Mice.

Int J Mol Sci

December 2024

Department of Biomedical and Pharmaceutical Sciences, Graduate School, Kyung Hee University, Seoul 02446, Republic of Korea.

The amount of sphingosine 1-phosphate (S1P) found in the synovial tissue of individuals with rheumatoid arthritis is five times greater than that in those with osteoarthritis. Our study aims to determine whether inhibiting S1P can mitigate collagen-induced rheumatoid arthritis (CIA) by using an S1P antagonist, JTE-013, alongside DBA-1J wild-type (WT) and knock-out (KO) mice. CIA causes increases in arthritis scores, foot swelling, synovial hyperplasia, pannus formation, proteoglycan depletion, cartilage damage, and bone erosion, but these effects are markedly reduced when JTE-013 is administered to WT mice.

View Article and Find Full Text PDF

Background: Chronic obstructive pulmonary disease (COPD) induces an imbalance in T helper (Th) 17/regulatory T (Treg) cells that contributes to of the dysregulation of inflammation. Exercise training can modulate the immune response in healthy subjects.

Objective: We aimed to evaluate the effects of exercise training on Th17/Treg responses and the differentiation of Treg phenotypes in individuals with COPD.

View Article and Find Full Text PDF

Want AI Summaries of new PubMed Abstracts delivered to your In-box?

Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!