ArticleFrontiers in immunology2024
The atypical chemokine receptor 2 reduces T cell expansion and tertiary lymphoid tissue but does not limit autoimmune organ injury in lupus-prone B6lpr mice.
Article in Frontiers in immunology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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Who cites it
3 citing papers in PubMed.
- Decoy Receptors in Autoimmunity: Molecular Guardians and Pathogenic Players in Immune Dysregulation.Mediators of inflammation · 2026Review
- Targeting the atypical chemokine receptor 2 (Oncoimmunology · 2025Article
- Selective expression and significance of ACKR2 in lung aerocytes.Journal for immunotherapy of cancer · 2025Article
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Authors and funding
3 authors.
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Abstract
Introduction: The atypical chemokine receptor 2 (ACKR2) is a chemokine scavenger receptor, which limits inflammation and organ damage in several experimental disease models including kidney diseases. However, potential roles of ACKR2 in reducing inflammation and tissue injury in autoimmune disorders like systemic lupus erythematosus (SLE) and lupus nephritis are unknown, as well as its effects on systemic autoimmunity. Methods: To characterize functional roles of ACKR2 in SLE, genetic Ackr2 deficiency was introduced into lupus-prone C57BL/6lpr (Ackr2-/- B6lpr) mice. Results: Upon inflammatory stimulation Discussion: In summary, we show that ACKR2 prevents expansion of T cells and formation of tertiary lymphoid tissue, but is not essential to limit autoimmune tissue injury in lupus-prone B6lpr mice.
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