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Related Concept Videos

Autoimmune Disorders01:29

Autoimmune Disorders

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Autoimmune diseases are a group of disorders in which the body's immune system mistakenly attacks its own cells, tissues, and organs. This results from an overactive immune response against substances and tissues normally present in the body. Let's delve into the concept and mechanism of autoimmune diseases from an immune system point of view, explore different causes and examples of such diseases, and discuss potential solutions.
Concept and Mechanism of Autoimmune Diseases
The immune...
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Genome-wide Association Studies-GWAS01:11

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Genome-wide association studies or GWAS are used to identify whether common SNPs are associated with certain diseases. Suppose specific SNPs are more frequently observed in individuals with a particular disease than those without the disease. In that case, those SNPs are said to be associated with the disease. Chi-square analysis is performed to check the probability of the allele likely to be associated with the disease.
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Skin is the first line of defense and encounters a variety of microbes. Some pathogenic strains are often the cause of a broad range of infections of the skin and other body systems. These conditions can affect people of all ages and may have different causes, including genetic factors, infections, autoimmune reactions, environmental factors, and lifestyle choices.
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Organisms are capable of detecting and fixing nucleotide mismatches that occur during DNA replication. This sophisticated process requires identifying the new strand and replacing the erroneous bases with correct nucleotides. Mismatch repair is coordinated by many proteins in both prokaryotes and eukaryotes.
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The JAK-STAT Signaling Pathway01:20

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Several cytokine receptors have tightly bound Janus kinase or JAK proteins attached at their cytosolic tail. Small signaling molecules such as cytokines, growth hormones, or prolactins bind to the cytokine receptors and initiate their dimerization. The dimerization brings the cytosolic JAKs together that trans-phosphorylate and activates each other. The activated JAKs now phosphorylate cytosolic tails of the cytokine receptors, which serve as binding sites for adaptor proteins such as  SH2...
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Related Experiment Video

Updated: Sep 13, 2025

Candidate Gene Testing in Clinical Cohort Studies with Multiplexed Genotyping and Mass Spectrometry
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Association between autoimmune diseases and keloids: a bidirectional two-sample Mendelian randomization study.

Dongshuo Ji1, Ying Liu1, Xing Han1

  • 1Plastic surgery Department, Beijing Hospital of Integrated Traditional Chinese and Western Medicine, Beijing, 100038, China.

European Journal of Dermatology : EJD
|July 31, 2025
PubMed
Summary

This study found no causal link between autoimmune diseases like rheumatoid arthritis and keloids. Mendelian randomization analysis confirmed that these conditions do not influence each other, suggesting separate underlying mechanisms.

Keywords:
autoimmune diseasesgenome-wide association studykeloidstwo-sample Mendelian randomization

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Area of Science:

  • Genetics
  • Immunology
  • Dermatology

Background:

  • Observational studies suggest a link between autoimmune diseases and keloids, but causality is unproven.
  • Investigating this association is crucial for understanding disease pathogenesis and potential therapeutic targets.

Purpose of the Study:

  • To determine the causal relationship between selected autoimmune diseases and keloids using a bidirectional Mendelian randomization approach.
  • To assess the potential causal effect of rheumatoid arthritis (RA), systemic lupus erythematosus (SLE), type 1 diabetes (T1D), and inflammatory bowel disease (IBD) subtypes (Crohn's disease and ulcerative colitis) on keloid development.

Main Methods:

  • Bidirectional two-sample Mendelian randomization (MR) analysis.
  • Utilized genome-wide association studies (GWAS) summary statistics.
  • Employed inverse-variance weighted (IVW) as the primary method, with weighted median, weighted mode, and MR-Egger regression for sensitivity analyses.
  • Assessed heterogeneity, pleiotropy, and outliers using Cochran's Q test, MR-Egger regression, and MR-PRESSO.

Main Results:

  • No statistically significant causal effect of genetically predicted autoimmune diseases on keloids was observed (e.g., RA: OR=0.95, p=0.07; SLE: OR=0.98, p=0.34).
  • Reverse MR analysis indicated no significant causal effect of keloids on autoimmune diseases.
  • Sensitivity analyses and heterogeneity/pleiotropy assessments supported the robustness of the findings.

Conclusions:

  • This MR study provides no strong evidence for a causal association between the investigated autoimmune diseases and keloids in the European population.
  • The findings suggest that observed links may be due to confounding factors rather than direct causality.