ArticleThe Journal of experimental medicine2019
A CCL1/CCR8-dependent feed-forward mechanism drives ILC2 functions in type 2-mediated inflammation.
Article in The Journal of experimental medicine, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 47 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
47 citing papers in PubMed.
- Interleukin-4-producing type 2 innate lymphoid cells in the lymph node promote proallergic Tfh13 cell differentiation.Immunity · 2026Article
- Metabolically reprogrammed eosinophils impair T cell immunity and cause chronic skin infection.EMBO molecular medicine · 2026Article
- Hidden immune memory niches in inflammatory skin diseases.bioRxiv : the preprint server for biology · 2026Article
- Single-cell analysis of recruited ILC2 cell fate during transition from circulation to establishment of tissue residency.Journal of immunology (Baltimore, Md. : 1950) · 2026Article
- Expansion of multiple CD4The Journal of allergy and clinical immunology · 2025Article
- Association of increased serum I-309 with renal function impairment and diabetic kidney disease in type 2 diabetes mellitus.Endocrine connections · 2025Article
- ILC2 Diversity, Location, and Function in Pulmonary Disease.Immunological reviews · 2025Review
- RAG suppresses group 2 innate lymphoid cells.eLife · 2025Article
- Association of increased serum I-309 with phenotypes, disease activity, and cytokine pattern in primary Sjögren's syndrome.Clinical rheumatology · 2025Article
- No bones about it: regulatory T cells promote fracture healing.The Journal of clinical investigation · 2025Article
- Succinate Facilitates CD4Journal of inflammation research · 2025Article
- Targeting the glucocorticoid receptor-CCR8 axis mediated bone marrow T cell sequestration enhances infiltration of anti-tumor T cells in intracranial cancers.Cellular & molecular immunology · 2024Article
- Review
- Progesterone amplifies allergic inflammation and airway pathology in association with higher lung ILC2 responses.American journal of physiology. Lung cellular and molecular physiology · 2024Article
- Lack of the IFN-γ signal leads to lethal Orientia tsutsugamushi infection in mice with skin eschar lesions.PLoS pathogens · 2024Article
- Development of a cellular model to study CCR8 signaling in tumor-infiltrating regulatory T cells.Cancer immunology, immunotherapy : CII · 2024Article
- Acute and chronic impact of interleukin-33 stimulation on chemokines and growth factors in human cord blood-derived mast cells.PloS one · 2024Article
- Cutting Edge: CCR8 Signaling Regulates IL-25- and IL-33-Responsive Skin Group 2 Innate Lymphoid Cell Migration and Function.Journal of immunology (Baltimore, Md. : 1950) · 2023Article
- Soybean (International journal of molecular sciences · 2023Article
- Group 2 innate lymphoid cells protect mouse heart from myocardial infarction injury via interleukin 5, eosinophils, and dendritic cells.Cardiovascular research · 2023Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
9 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Group 2 innate lymphoid cells (ILC2s) possess indispensable roles during type 2-mediated inflammatory diseases. Although their physiological and detrimental immune functions seem to depend on the anatomical compartment they reside, their tissue tropism and the molecular and immunological processes regulating the self-renewal of the local pool of ILC2s in the context of inflammation or infection are incompletely understood. Here, we analyzed the role of the CC-chemokine receptor CCR8 for the biological functions of ILC2s. In vitro and in vivo experiments indicated that CCR8 is in comparison to the related molecule CCR4 less important for migration of these cells. However, we found that activated mouse and human ILC2s produce the CCR8 ligand CCL1 and are a major source of CCL1 in vivo. CCL1 signaling to ILC2s regulates their proliferation and supports their capacity to protect against helminthic infections. In summary, we identify a novel chemokine receptor-dependent mechanism by which ILC2s are regulated during type 2 responses.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.