ArticleArthritis research & therapy2015
Phosphatase and tensin homolog (PTEN) in antigen-presenting cells controls Th17-mediated autoimmune arthritis.
Article in Arthritis research & therapy, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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Who cites it
17 citing papers in PubMed, 32 citations in OpenAlex.
- PTEN-mediated resistance in cancer: From foundation to future therapies.Toxicology reports · 2025Review
- Proteomic Profile Regulated by the Immunomodulatory Jusvinza Drug in Neutrophils Isolated from Rheumatoid Arthritis Patients.Biomedicines · 2024Article
- PTEN: an emerging target in rheumatoid arthritis?Cell communication and signaling : CCS · 2024Review
- Pre-Activated Granulocytes from an Autoimmune Uveitis Model Show Divergent Pathway Activation Profiles upon IL8 Stimulation In Vitro.International journal of molecular sciences · 2022Article
- The phosphatase PTEN links platelets with immune regulatory functions of mouse T follicular helper cells.Nature communications · 2022Article
- Aryl hydrocarbon receptor (Ahr)-dependent Il-22 expression by type 3 innate lymphoid cells control of acute joint inflammation.Journal of cellular and molecular medicine · 2021Article
- The Role of PTEN in Innate and Adaptive Immunity.Cold Spring Harbor perspectives in medicine · 2019Review
- PTEN Hamartoma Tumor Syndrome and Immune Dysregulation.Translational oncology · 2019Review
- Effects of Th17 cells and IL-17 in the progression of cervical carcinogenesis with high-risk human papillomavirus infection.Cancer medicine · 2018Article
- PTEN drives Th17 cell differentiation by preventing IL-2 production.The Journal of experimental medicine · 2017Article
- Ssu72 attenuates autoimmune arthritis via targeting of STAT3 signaling and Th17 activation.Scientific reports · 2017Article
- The functions of tumor suppressor PTEN in innate and adaptive immunity.Cellular & molecular immunology · 2017Review
- Rheumatoid Arthritis Fibroblast-like Synoviocyte Suppression Mediated by PTEN Involves Survivin Gene Silencing.Scientific reports · 2017Article
- Emerging roles of p53 and other tumour-suppressor genes in immune regulation.Nature reviews. Immunology · 2016Review
- Myeloid PTEN deficiency impairs tumor-immune surveillance via immune-checkpoint inhibition.Oncoimmunology · 2016Article
- Review
- Negative regulation of TLR signaling in myeloid cells--implications for autoimmune diseases.Immunological reviews · 2016Review
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Authors and funding
16 authors at 3 institutions in 2 countries.
Funding
Abstract
introductionAutoreactive T cells are a central element in many systemic autoimmune diseases. The generation of these pathogenic T cells is instructed by antigen-presenting cells (APCs). However, signaling pathways in APCs that drive autoimmune diseases, such as rheumatoid arthritis, are not understood.
methodsWe measured phenotypic maturation, cytokine production and induction of T cell proliferation of APCs derived from wt mice and mice with a myeloid-specific deletion of PTEN (myeloid PTEN(-/-)) in vitro and in vivo. We induced collagen-induced arthritis (CIA) and K/BxN serum transfer arthritis in wt and myeloid-specific PTEN(-/-) mice. We measured the cellular composition of lymph nodes by flow cytometry and cytokines in serum and after ex vivo stimulation of T cells.
resultsWe show that myeloid-specific PTEN(-/-) mice are almost protected from CIA. Myeloid-specific deletion of PTEN leads to a significant reduction of cytokine expression pivotal for the induction of systemic autoimmunity such as interleukin (IL)-23 and IL-6, leading to a significant reduction of a Th17 type of immune response characterized by reduced production of IL-17 and IL-22. In contrast, myeloid-specific PTEN deficiency did not affect K/BxN serum transfer arthritis, which is independent of the adaptive immune system and solely depends on innate effector functions.
conclusionsThese data demonstrate that the presence of PTEN in myeloid cells is required for the development of CIA. Deletion of PTEN in myeloid cells inhibits the development of autoimmune arthritis by preventing the generation of a pathogenic Th17 type of immune response.
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