Unraveling the Link between Air Pollution and Psoriasis Subtypes: Genetic Architecture of Epigenetic Insights and Mediating Cytokines.

The impact of air pollution on psoriasis is poorly understood. We conducted a prospective cohort study and used epigenetic Mendelian randomization (MR) to dissect the pathogenic effects of air pollution. We first investigated the associations between air pollution and the incidence of skin psoriasis and psoriatic arthritis (PsA) within the UK Biobank cohort.

Unseen Threats: The Impact of Relatively Low-Level Ambient Air Pollution on Autoimmune Diseases.

In developing countries like China, personal air-purifying respirators and indoor air purifiers are commonly used to mitigate high levels of air pollution, whereas lower pollution levels in many developed countries lead to less proactive measures. However, emerging evidence suggests that even relatively low-level air pollution can elevate the risk of autoimmune diseases. Recent biobank studies demonstrated a linear relationship between chronic exposure to relatively low-level ambient air pollution and the incidence of autoimmune diseases, particularly in genetically susceptible populations.

Revisiting the role of GDF15 in atherosclerosis in mouse and human.

Growth differentiation factor 15 (GDF15) is a key regulator of food intake and energy metabolism. GDF15 mimetic drugs for the treatment of metabolic syndrome and obesity are under clinical development. While GDF15 presents a promising target for weight management, its potential cardiovascular actions remain elusive.

Serum folate levels and the risk of psoriasis: evidence from observational study and Mendelian randomisation.

This study aimed to investigate the relationship between serum folate levels and the risk of psoriasis by integrating observational study with Mendelian Randomisation (MR) analysis. We firstly conducted an observational study using data from the National Health and Nutrition Examination Survey (NHANES). Subsequently, genetic instruments were selected for two-sample MR analyses to investigate the causal relationship between serum folate levels and the risk of psoriasis.

In vitro silencing of RIP2 in naive CD4 T cells from lupus-prone mice promotes pathogenic Th17 cell differentiation.

Objective: This work aims to investigate whether RIP2 silencing in naive CD4 T cells from lupus-prone mice impacts Th17 cell activity or differentiation in vitro.

Methods: Naive CD4 T cells isolation from MRL/lpr mice's spleens. Three RNA interference target sequences of RIP2 were packaged with lentivirus and transfected into naive CD4 T cells.

Genetically predicted circulating interleukin-18 levels are associated with risk of systemic lupus erythematosus and type 1 diabetes.

Objective: Interleukin-18 (IL-18) is a proinflammatory cytokine. This study aims to determine whether there is a causal relationship between circulating IL-18 concentrations and the risk of inflammatory and autoimmune diseases.

Methods: We collected significant single nucleotide polymorphisms (SNPs) associated with circulating IL-18 levels ( < 5 × 10) as instrumental variables (IVs) from a genome-wide association study (GWAS) involving 21,758 individuals of European descent.

Effects of alcohol on the composition and metabolism of the intestinal microbiota among people with HIV: A cross-sectional study.

Objectives: Alcohol consumption is not uncommon among people with HIV (PWH) and may exacerbate HIV-induced intestinal damage, and further lead to dysbiosis and increased intestinal permeability. This study aimed to determine the changes in the fecal microbiota and its association with alcohol consumption in HIV-infected patients.

Methods: A cross-sectional survey was conducted between November 2021 and May 2022, and 93 participants were recruited.

RIPK2 as a promising druggable target for autoimmune diseases.

Receptor Interacting Serine/Threonine Kinase 2 (RIPK2) is an essential regulator of the inflammatory process and immune response. In innate immunity, the NOD-RIPK2 signaling axis is an important pathway that directly mediates inflammation and immune response. In adaptive immunity, RIPK2 may affect T cell proliferation, differentiation and cellular homeostasis thereby involving T cell-driven autoimmunity, but the exact mechanism remains unclear.

Association of Combined Exposure to Ambient Air Pollutants, Genetic Risk, and Incident Rheumatoid Arthritis: A Prospective Cohort Study in the UK Biobank.

Background: Evidence for a potential link between air pollution and rheumatoid arthritis (RA) is inconsistent, and the modified effect of genetic susceptibility on the relationship between air pollution and RA has not been well studied.

Objective: Using a general population cohort from the UK Biobank, this study aimed to investigate the associations between various air pollutants and the risk of incident RA and to further estimate the impact of combined exposure to ambient air pollutants on the risk of developing RA under the modification effect of genetic predisposition.

Methods: A total of 342,973 participants with completed genotyping data and who were free of RA at baseline were included in the study.

Altered gut fungi in systemic lupus erythematosus - A pilot study.

Objective: Gut fungi, as symbiosis with the human gastrointestinal tract, may regulate physiology multiple interactions with host cells. The plausible role of fungi in systemic lupus erythematosus (SLE) is far from clear and need to be explored.

Methods: A total of 64 subjects were recruited, including SLE, rheumatoid arthritis (RA), undifferentiated connective tissue diseases (UCTDs) patients and healthy controls (HCs).

Telomere Length and Development of Systemic Lupus Erythematosus: A Mendelian Randomization Study.

Objective: Previous observational studies demonstrated that a subset of patients with systemic lupus erythematosus (SLE) have markedly short telomere length in leukocytes. This study was undertaken to test whether leukocyte telomere length is causally associated with risk of SLE.

Methods: A 2-sample Mendelian randomization (MR) analysis was conducted to estimate causality of telomere length on SLE in European populations.

The Interaction Between Dietary Fructose and Gut Microbiota in Hyperuricemia and Gout.

With the worldwide epidemics of hyperuricemia and associated gout, the diseases with purine metabolic disorders have become a serious threat to human public health. Accumulating evidence has shown that they have been linked to increased consumption of fructose in humans, we hereby made a timely review on the roles of fructose intake and the gut microbiota in regulating purine metabolism, together with the potential mechanisms by which excessive fructose intake contributes to hyperuricemia and gout. To this end, we focus on the understanding of the interaction between a fructose-rich diet and the gut microbiota in hyperuricemia and gout to seek for safe, cheap, and side-effect-free clinical interventions.

ALKBH5 Expression could Affect the Function of T Cells in Systemic Lupus Erythematosus Patients: A Case-control Study.

Background: N6-methyladenosine (m6A) modification is widespread in eukaryotic mRNA, regulated by m6A demethylase, AlkB homolog 5 (ALKBH5). However, the role of m6A in systemic lupus erythematosus (SLE) is still obscure. We explored ALKBH5 expression in SLE patients and its effects on T cells.

Biological insights into systemic lupus erythematosus through an immune cell-specific transcriptome-wide association study.

Objective: Genome-wide association studies (GWAS) have identified >100 risk loci for systemic lupus erythematosus (SLE), but the disease genes at most loci remain unclear, hampering translation of these genetic discoveries. We aimed to prioritise genes underlying the 110 SLE loci that were identified in the latest East Asian GWAS meta-analysis.

Methods: We built gene expression predictive models in blood B cells, CD4 and CD8 T cells, monocytes, natural killer cells and peripheral blood cells of 105 Japanese individuals.

Involvement of N6-methyladenosine modifications of long noncoding RNAs in systemic lupus erythematosus.

Background: LncRNAs are potential biomarkers for SLE, but the epigenetic regulatory mechanisms of N6-methyladenosine (m6A) modification in SLE remain largely unclear.

Methods: In this study, we established m6A modification profile and investigated the potential roles of m6A-related lncRNAs in SLE. The m6A modification profile of SLE was established using MeRIP-seq.

Meta-analysis of 208370 East Asians identifies 113 susceptibility loci for systemic lupus erythematosus.

Objective: Systemic lupus erythematosus (SLE), an autoimmune disorder, has been associated with nearly 100 susceptibility loci. Nevertheless, these loci only partially explain SLE heritability and their putative causal variants are rarely prioritised, which make challenging to elucidate disease biology. To detect new SLE loci and causal variants, we performed the largest genome-wide meta-analysis for SLE in East Asian populations.

Identification of new susceptibility loci associated with rheumatoid arthritis.

Objectives: The present study aimed to discover novel susceptibility loci associated with risk of rheumatoid arthritis (RA).

Methods: We performed a new genome-wide association study (GWAS) in Chinese subjects (1027 RA cases and 2879 controls) and further conducted an expanded meta-analysis with previous GWAS summary data and replication studies. The functional roles of the associated loci were interrogated using publicly available databases.

Review on the Alteration of Gut Microbiota: The Role of HIV Infection and Old Age.

Human immunodeficiency virus (HIV) infection results in gut microbiota alteration and this is associated with immune activation and chronic inflammation. The gastrointestinal tract is a primary site of viral replication and thus HIV-induced loss of T-helper (Th) cells in the gut causes impairments in intestinal barriers, resulting in disruptions in intestinal immunity and precipitating into gut dysbiosis. Here, we show that late HIV diagnosis can negatively affect the immunological, virological, and clinical prognosis of the patients with its higher implication at an older age.

Decreased H19, GAS5, and linc0597 Expression and Association Analysis of Related Gene Polymorphisms in Rheumatoid Arthritis.

Long noncoding RNAs (lncRNAs) widely participate in human diseases by regulating gene transcription, modulating protein function, or acting as ceRNAs. Yet, their roles in rheumatoid arthritis (RA) remain obscure. In this study, the expression of three lncRNAs (H19, GAS5, and linc0597) in peripheral blood mononuclear cells (PBMCs) were detected in 77 RA patients and 78 controls using quantitative real-time reverse transcription polymerase chain reaction (qRT-PCR).

Discovery of new serum biomarker panels for systemic lupus erythematosus diagnosis.

Objective: Clinical diagnosis of SLE is currently challenging due to its heterogeneity. Many autoantibodies are associated with SLE and are considered potential diagnostic markers, but systematic screening and validation of such autoantibodies is lacking. This study aimed to systematically discover new autoantibodies that may be good biomarkers for use in SLE diagnosis.

Expression of several long noncoding RNAs in peripheral blood mononuclear cells of patients with systemic lupus erythematosus.

Purpose: Accumulating evidence has linked long noncoding RNAs (lncRNAs) to autoimmune and inflammatory disorders. This study aimed to detect the expression levels of five lncRNAs (lnc0640, lnc3643, lnc5150, lnc7514 and lncagf) in peripheral blood mononuclear cells (PBMCs) of patients with systemic lupus erythematosus (SLE), as well as their correlation with clinical and laboratory features.

Materials/methods: We recruited 76 patients with SLE and 71 normal controls into the present study, and obtained PBMCs from the blood samples of all study subjects.

TREX1 As a Potential Therapeutic Target for Autoimmune and Inflammatory Diseases.

Background And Objectives: The 3' repair exonuclease 1 (TREX1) gene is the major DNA-specific 3'-5 'exonuclease of mammalian cells which reduces single- and double-stranded DNA (ssDNA and dsDNA) to prevent undue immune activation mediated by the nucleic acid. TREX1 is also a crucial suppressor of selfrecognition that protects the host from inappropriate autoimmune activations. It has been revealed that TREX1 function is necessary to prevent host DNA accumulating after cell death which could actuate an autoimmune response.