Silica's silent threat: Contributing to skin fibrosis in systemic sclerosis by targeting the HDAC4/Smad2/3 pathway.

Nowadays, silica products are widely used in daily life, especially in skin applications, which inevitably increases the risk of silica exposure in general population. However, inadequate awareness of silica's potential hazards and lack of self-protection are of concern. Systemic sclerosis (SSc) is characterized by progressive tissue fibrosis under environmental and genetic interactions.

The Price of Beauty: A Literature Review on Non-Tuberculous Mycobacteria Infection After Cosmetic Procedures.

Non-tuberculous mycobacteria (NTM) infection of the skin and soft tissues is a complication of cosmetic procedures. The incidence of cutaneous NTM infections has increased significantly as aesthetic operations have become more commonplace. With the rise of cosmetic tourism, the geographic expansion of NTM infections is a major concern.

Sirtuin 1 overexpression contributes to the expansion of follicular helper T cells in systemic lupus erythematosus and may serve as an accessible therapeutic target.

Objective: SIRT1, an NAD+-dependent deacetylase, is upregulated in CD4+ T cells from SLE patients and MRL/lpr lupus-like mice. This study aimed to explore the role of SIRT1 in follicular helper T (Tfh) cell expansion and its potential value as a therapeutic target for SLE.

Methods: Frequencies of CD4+CXCR5+PD-1+ Tfh cells in peripheral blood from SLE patients and their expression of SIRT1 and B cell lymphoma 6 (BCL-6) were determined with flow cytometry.

ATRA ameliorates fibrosis by suppressing the pro-fibrotic molecule Fra2/AP-1 in systemic sclerosis.

Systemic sclerosis (SSc) is an autoimmune connective tissue disease that leads to irreversible fibrosis of the skin and the internal organs. The etiology of SSc is complex, its pathophysiology is poorly understood, and clinical therapeutic options are restricted. Thus, research into medications and targets for treating fibrosis is essential and urgent.

Activating Protein-1 (AP-1): A Promising Target for the Treatment of Fibrotic Diseases.

The fibrosis of tissues and organs occurs via an aberrant tissue remodeling process characterized by an excessive deposition of extracellular matrix, which can lead to organ dysfunction, organ failure, and death. Because the pathogenesis of fibrosis remains unclear and elusive, there is currently no medication to reverse it; hence, this process deserves further study. Activating protein-1 (AP-1)-comprising Jun (c-Jun, JunB, JunD), Fos (c-fos, FosB, Fra1, and Fra2), and activating transcription factor-is a versatile dimeric transcription factor.

UVA1 irradiation attenuates collagen production via Ficz/AhR/MAPK signaling activation in scleroderma.

Scleroderma is an autoimmune disease mainly characterized by progressive fibrosis of the skin. There are two types of scleroderma, namely localized scleroderma (LS) and systemic sclerosis (SSc); skin lesions in both types of scleroderma are histologically identical. Progressive skin sclerosis induces psychological and ecological burden for scleroderma patients.

Overexpressed perforin contributes to the melanocyte destruction via epigenetic regulation in patients with vitiligo.

Background: Perforin (PRF), a pivotal cytotoxic effector molecule of activated CD8 T cells, has a crucial role in the pathogenesis of vitiligo. However, the mechanisms leading to the abnormal perforin expression remain poorly understood in the CD8 T cells of vitiligo patients.

Objective: To investigate the contributions of DNA methylation to the abnormal expression of perforin in CD8 T cells of vitiligo patients.

Bullous lichen sclerosus-generalized morphea overlap syndrome improved by tofacitinib.

We here report a case of a middle-aged man with an unusual case of bullous lichen sclerosus complicated with generalized morphea. He showed initial recurrent flaccid bullae, followed by ivory-white sclerotic plaques and extensive skin sclerosis, with additional walking disorder caused by knee-joint contracture, and ulcers on the lower extremities and back. The patient had no visceral involvement.

Overexpression of OASL upregulates TET1 to induce aberrant activation of CD4 T cells in systemic sclerosis via IRF1 signaling.

Background: Systemic sclerosis (SSc), an autoimmune disease with unknown etiology and pathogenesis, is characterized by abnormal autoimmunity, vascular dysfunction, and progressive fibrosis of skin and organs. Studies have shown that a key factor in the pathogenesis of SSc is aberrant activation of CD4 T cells. Our previous studies have shown that a global hypomethylation state of CD4 T cells is closely related to aberrant activation.

Esomeprazole alleviates fibrosis in systemic sclerosis by modulating AhR/Smad2/3 signaling.

Systemic sclerosis (SSc) is a connective tissue disease with the involvement of complex signaling pathways, such as TGF-β/Smad2/3. SSc can lead to severe multiple organ fibrosis, but no effective therapy is currently available because of its unclear pathogenesis. Exploring new treatments is the focus of recent research on SSc.

High expression of VTRNA2-1 in systemic lupus erythematosus patients' B lymphocytes and its significance.

Objectives: To investigate the expression of vault ribonucleic acid 2-1 (VTRNA2-1) in T or B lymphocytes in patients with systemic lupus erythematosus (SLE) from the perspective of epigenetic non-coding RNA, and to explore the preliminary pathogenesis of SLE.

Methods: CD4 T lymphocytes from peripheral blood in 25 healthy controls and 32 SLE patients, CD19 B lymphocytes from peripheral blood in 62 SLE patients (47 patients were active SLE and 15 patients were inactive) and 29 healthy controls were collected, and the expression levels of VTRNA2-1 were detected by real-time PCR. Co-immunoprecipitation assay was used to explore the direct-acting proteins of VTRNA2-1.

[Clinical analysis for 108 cases of dermatomyositis].

To investigate the clinical characteristics of dermatomyositis, to investigate the types and clinical features of dermatomyositis complicated with malignant tumor, and to provide evidence for clinical diagnosis, treatment and prognostic evaluation.
 Methods: The clinical manifestations and laboratory test results for 108 cases of dermatomyositis with complications in the Second Xiangya Hospital of Central South University were analyzed.
 Results: Patients aged from 14 to 60 years accounted for 62.

The role of microRNA-1246 in the regulation of B cell activation and the pathogenesis of systemic lupus erythematosus.

Background: The pathogenesis of systemic lupus erythematosus (SLE) has not yet been completely elucidated. One of the hallmarks of SLE is the production of autoantibodies by uncontrolled over-activated B cells. Early B cell factor 1 (EBF1) contributes to the development, activation, and proliferation of B cells through activation of the AKT signaling pathway.

Acquired hemophilia associated with bullous pemphigoid: a case report.

The development of factor VIII inhibitors in non-hemophilic patients is rare and may occur in healthy individuals, mostly elderly and women in postpartum period, and in patients with malignant neoplasia or autoimmune diseases, such as bullous pemphigoid. We described the case of a 60-year-old female patient who developed bullous pemphigoid for 3 month and presented with bleeding tendency and hematoma in the tongue. Therapy with methylprednisolone, cyclophosphamide, intravenous immunoglobulin and factor VIII reposition was instituted, resulting in a remission of the bleeding and negativity for antibodies against factor VIII titers.

Creating a flexible multiple microRNA expression vector by linking precursor microRNAs.

MicroRNAs (miRNAs) are ∼22nt non-coding RNA molecules that usually function as endogenous repressors of target genes. Many biological processes depend on faithful miRNA expression and miRNA profiling has revealed dysregulation of many miRNAs in neurological, and cardiovascular diseases, and in cancer. Despite this finding, most studies have focused on the function of single miRNAs or miRNA clusters.

Equitoxic doses of 5-azacytidine and 5-aza-2'deoxycytidine induce diverse immediate and overlapping heritable changes in the transcriptome.

Background: The hypomethylating agent 5-Azacytidine (5-Aza-CR) is the first drug to prolong overall survival in patients with myelodysplastic syndrome (MDS). Surprisingly, the deoxyribonucleoside analog 5-Aza-2'deoxycytidine (5-Aza-CdR) did not have a similar effect on survival in a large clinical trial. Both drugs are thought to exert their effects after incorporation into DNA by covalent binding of DNA methyltransferase (DNMT).

S110, a 5-Aza-2'-deoxycytidine-containing dinucleotide, is an effective DNA methylation inhibitor in vivo and can reduce tumor growth.

Methylation of CpG islands in promoter regions is often associated with gene silencing and aberrant DNA methylation occurs in most cancers, leading to the silencing of some tumor suppressor genes. Reversal of this abnormal hypermethylation by DNA methylation inhibitors is effective in reactivating methylation-silenced tumor suppressor genes both in vitro and in vivo. Several DNA methylation inhibitors have been well studied; the most potent among them is 5-aza-2'-deoxycytidine (5-Aza-CdR), which can induce myelosuppression in patients.

T cell CD40LG gene expression and the production of IgG by autologous B cells in systemic lupus erythematosus.

CD40 ligand (CD40LG), encoded on the X chromosome, has been reported to be overexpressed on lupus T cells. Herein, we investigated the effect of DNA demethylation on T cell CD40LG expression and the production of IgG by autologous B cells in lupus. We found normal human T cells transfected with CD40LG induced autologous B cell activation and plasma cell differentiation.