ArticleNature communications2021
Polymorphic estrogen receptor binding site causes Cd2-dependent sex bias in the susceptibility to autoimmune diseases.
Article in Nature communications, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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Who cites it
14 citing papers in PubMed, 30 citations in OpenAlex.
- Dysfunctional decidual CD2Frontiers in immunology · 2026Article
- Estrogen and progesterone-mediated differential modulation of CD4Frontiers in immunology · 2026Article
- The sex-biased chromatin modifier SMC1A promotes autoimmunity by shaping inflammatory pathways in patients with SLE.Nature communications · 2025Article
- Article
- Epigenetic remodeling by sex hormone receptors and implications for gender affirming hormone therapy.Frontiers in immunology · 2025Review
- Generation and characterization of a tamoxifen-inducible lineage tracing toolFrontiers in immunology · 2025Article
- The role of immunoglobulin E in non-atopic disorders.Frontiers in immunology · 2025Review
- The Impact of Microbiota-Immunity-Hormone Interactions on Autoimmune Diseases and Infection.Biomedicines · 2024Review
- Identification of hub genes and transcription factors in patients with primary gout complicated with atherosclerosis.Scientific reports · 2024Article
- Self-reactive IgE and anti-IgE therapy in autoimmune diseases.Frontiers in pharmacology · 2023Review
- Sex chromosome complement and sex steroid signaling underlie sex differences in immunity to respiratory virus infection.Frontiers in pharmacology · 2023Review
- Article
- Sex bias in lymphocytes: Implications for autoimmune diseases.Frontiers in immunology · 2022Review
- The commonness in immune infiltration of rheumatoid arthritis and atherosclerosis: Screening for central targetsFrontiers in immunology · 2022Article
Corrections and comments
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Authors and funding
10 authors at 3 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Complex autoimmune diseases are sexually dimorphic. An interplay between predisposing genetics and sex-related factors probably controls the sex discrepancy in the immune response, but the underlying mechanisms are unclear. Here we positionally identify a polymorphic estrogen receptor binding site that regulates Cd2 expression, leading to female-specific differences in T cell-dependent mouse models of autoimmunity. Female mice with reduced Cd2 expression have impaired autoreactive T cell responses. T cells lacking Cd2 costimulation upregulate inhibitory Lag-3. These findings help explain sexual dimorphism in human autoimmunity, as we find that CD2 polymorphisms are associated with rheumatoid arthritis and 17-β-estradiol-regulation of CD2 is conserved in human T cells. Hormonal regulation of CD2 might have implications for CD2-targeted therapy, as anti-Cd2 treatment more potently affects T cells in female mice. These results demonstrate the relevance of sex-genotype interactions, providing strong evidence for CD2 as a sex-sensitive predisposing factor in autoimmunity.
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