Background: Primary Sjögren Syndrome (pSS) is a chronic autoimmune disease characterized by epithelial atrophy, mononuclear infiltration in exocrine glands resulting in the defective function of these glands. In pSS, atrophy of the epithelium is caused by an increased amount of apoptosis.

Objective: The main aim of this study is to investigate the role of the apoptosis-related factors by studying Bcl-2, Fas and FasL expression in relation to the extent of inflammation as well as the effect of therapy on the expression of these mediators.

Methods: In pSS patients (n=62) documented for their serological and clinical features, Fas, FasL and Bcl-2 plasma levels were assessed using enzyme-linked immunosorbent assays. In the same context, we investigated their expression by immunohistochemistry analysis in the labial salivary glands samples in association with the extent of inflammation.

Results: Interestingly, our results indicated that in pSS patients, the plasmatic Bcl-2, Fas and FasL levels, which appeared to be associated with the severity of inflammation and were significantly elevated in comparison to the healthy controls. Moreover, a significant decrease in all these factors was observed in patients after combined corticosteroids-hydroxychloroquine therapy. Importantly, we report a strong positive correlation between Bcl-2 and NO levels. The immunohistochemical staining reveals a strong Bcl-2 expression in infiltrating mononuclear cells and a total absence in the acinar cells. The Bcl-2 level varies according to the severity of pathology. However, the expression of Fas and FasL was less important and predominantly localized in infiltrating mononuclear cells.

Conclusion: Our current study highlights the involvement of Bcl-2, Fas and FasL in pSS glands injury. These factors may act as useful predictor markers of a clinical course in pSS, suggesting a novel approach in the pSS patients monitoring.

Download full-text PDF

Source
http://dx.doi.org/10.2174/1871530321666210809155147DOI Listing

Publication Analysis

Top Keywords

fas fasl
24
bcl-2 fas
16
pss patients
12
bcl-2
8
fasl levels
8
labial salivary
8
salivary glands
8
infiltrating mononuclear
8
pss
7
fas
6

Similar Publications

Silymarin: a promising modulator of apoptosis and survival signaling in cancer.

Discov Oncol

January 2025

Department of Biotechnology, School of Bio Sciences and Technology (SBST), Vellore Institute of Technology (VIT), Vellore, 632014, India.

Cancer, one of the deadliest diseases, has remained the epicenter of biological research for more than seven decades. Yet all the efforts for a perfect therapeutic cure come with certain limitations. The use of medicinal plants and their phytochemicals as therapeutics has received much attention in recent years.

View Article and Find Full Text PDF

Norepinephrine (NE) promotes activated B cells to identify and kill effector CD8 T cells through FasL/Fas pathway in spleen mononuclear cells isolated from experimental autoimmune encephalomyelitis (EAE).

Brain Behav Immun

January 2025

Department of Neurobiology, School of Basic Medical Sciences, Harbin Medical University, Harbin 150081, Heilongjiang, PR China; The Key Laboratory of Myocardial Ischemia, Harbin Medical University, Ministry of Education, Harbin 150081, Heilongjiang, PR China. Electronic address:

It has been reported that the nervous system can regulate immune reactions through various mechanisms. However, the role of splenic sympathetic nerve activity in the autoimmune reactions during the pathogenesis of experimental autoimmune encephalomyelitis (EAE) remained unclear. Here, we blocked the activity of the splenic sympathetic nerve and found that the number of adaptive immune cells, such as CD4 T cells, CD8 T cells and B cells, were upregulated.

View Article and Find Full Text PDF

While inputs regulating CD4 T helper cell (Th) differentiation are well-defined, the integration of downstream signaling with transcriptional and epigenetic programs that define Th-lineage identity remain unresolved. PI3K signaling is a critical regulator of T cell function; activating mutations affecting PI3Kδ result in an immunodeficiency with multiple T cell defects. Using mice expressing activated-PI3Kδ, we found aberrant expression of proinflammatory Th1-signature genes under Th2-inducing conditions, both and .

View Article and Find Full Text PDF

FAP-targeted radioligand therapy with Ga/Lu-DOTA-2P(FAPI) enhance immunogenicity and synergize with PD-L1 inhibitors for improved antitumor efficacy.

J Immunother Cancer

January 2025

Department of Nuclear Medicine and Minnan PET Center, Xiamen Cancer Center, The First Affiliated Hospital of Xiamen University, School of Medicine, Xiamen University, Xiamen, Fujian, China

Background: Fibroblast activation protein (FAP)-targeted radioligand therapy, with immunomodulatory effects, has shown efficacy in both preclinical and clinical studies. We recently reported on a novel dimeric FAP-targeting radiopharmaceutical, Ga/Lu-DOTA-2P(FAPI), which demonstrated increased tumor uptake and prolonged retention in various cancers. However, further exploration is required to understand the therapeutic efficacy and underlying mechanisms of combining Ga/Lu-DOTA-2P(FAPI) radioligand therapy with PD-1/PD-L1 immunotherapy.

View Article and Find Full Text PDF

Benzophenone-3 (BP-3), commonly used as a UV filter in personal care products and as a stabilizer, is an alleged endocrine disruptor with potential neurodevelopmental impacts. Despite its abundance in the environment, the studies on its effect on brain development are scarce, especially in terms of multigenerational impact. In this work, for the first time, we examined neurotoxic and pro-apoptotic effects of BP-3 on mouse brain regions (cerebral cortex and hippocampus) in both the first (F) and second (F) generations after maternal exposure to environmentally relevant BP-3 levels.

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!