Article in European journal of immunology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers, 1 of them a synthesis that pooled it.
0numbers the graph read from it
0cells of the map it votes in
3citing papers in PubMed, 1 pooled it
2.6field-weighted citation impact, top 10% of its field
1 · What the graph read from it
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.
2 · The registry
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.
3 · Its place in the literature
Who cites it
3 citing papers in PubMed, 1 synthesis or guideline pooled it, 11 citations in OpenAlex.
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
5 · Who and what money
Authors and funding
8 authors at 3 institutions in 2 countries.
Charline SommerFraunhofer Institute for Toxicology and Experimental Medicine ITEM, Biomedical Research in Endstage and Obstructive Lung Disease Hannover (BREATH), Member of the German Center for Lung Research (DZL), Member of the Fraunhofer Cluster of Excellence Immune-Mediated Diseases CIMD, Hannover, Germany.ORCID 0000-0002-6390-3878
Jarish N CohenDepartment of Dermatology, University of California, San Francisco, California, USA.
Susann DehmelFraunhofer Institute for Toxicology and Experimental Medicine ITEM, Biomedical Research in Endstage and Obstructive Lung Disease Hannover (BREATH), Member of the German Center for Lung Research (DZL), Member of the Fraunhofer Cluster of Excellence Immune-Mediated Diseases CIMD, Hannover, Germany.ORCID 0000-0003-4860-2767
Vanessa NeuhausFraunhofer Institute for Toxicology and Experimental Medicine ITEM, Biomedical Research in Endstage and Obstructive Lung Disease Hannover (BREATH), Member of the German Center for Lung Research (DZL), Member of the Fraunhofer Cluster of Excellence Immune-Mediated Diseases CIMD, Hannover, Germany.ORCID 0000-0002-0947-4929
Dirk SchaudienFraunhofer Institute for Toxicology and Experimental Medicine ITEM, Biomedical Research in Endstage and Obstructive Lung Disease Hannover (BREATH), Member of the German Center for Lung Research (DZL), Member of the Fraunhofer Cluster of Excellence Immune-Mediated Diseases CIMD, Hannover, Germany.ORCID 0000-0001-7398-7262
Armin BraunFraunhofer Institute for Toxicology and Experimental Medicine ITEM, Biomedical Research in Endstage and Obstructive Lung Disease Hannover (BREATH), Member of the German Center for Lung Research (DZL), Member of the Fraunhofer Cluster of Excellence Immune-Mediated Diseases CIMD, Hannover, Germany.
Katherina SewaldFraunhofer Institute for Toxicology and Experimental Medicine ITEM, Biomedical Research in Endstage and Obstructive Lung Disease Hannover (BREATH), Member of the German Center for Lung Research (DZL), Member of the Fraunhofer Cluster of Excellence Immune-Mediated Diseases CIMD, Hannover, Germany.ORCID 0000-0002-7804-4527
Michael D RosenblumDepartment of Dermatology, University of California, San Francisco, California, USA.
Fraunhofer Institute for Toxicology and Experimental Medicine · DEUniversity of California, San Francisco · USMedizinische Hochschule Hannover · DE
Funding
Research BaseP30DK063720 · NIDDK · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI GERMAN, MICHAEL S · 2003 to 2019
$21.8M
UCSF Dermatology Training GrantT32AR007175 · NIAMS · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI Wilson Liao, Michael David Rosenblum · 1986 to 2026
$6.1M
Restoring Immune Balance in Hiddradenitis SuppurativaR01AR075864 · NIAMS · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI ROSENBLUM, MICHAEL DAVID · 2020 to 2024
$3.5M
Elucidating the Role of Regulatory T cells in Establishing and Maintaining a Th2 Niche in SkinR01AR077553 · NIAMS · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI ROSENBLUM, MICHAEL DAVID · 2020 to 2024
$3.5M
Elucidating the Cellular and Molecular Mechanisms of How Regulatory T cells in Skin Regulate Fibroblast Activation and Tissue FibrosisR01AR071944 · NIAMS · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI ROSENBLUM, MICHAEL DAVID · 2018 to 2022
$1.7M
Elucidating the Role of Regulatory T cells in Protecting Epithelial Stem Cell NichesK08AR079596 · NIAMS · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI Jarish Newman Cohen · 2022 to 2026
$882k
BD FACSAria Fusion Cell SorterS10OD021822 · OD · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI LEE, MICHAEL R. · 2016 to 2016
Recombinant human IL-2 has been used to treat inflammatory diseases and cancer; however, side effects like skin rashes limit the use of this therapeutic. To identify key molecules and cells inducing this side effect, we characterized IL-2-induced cutaneous immune reactions and investigated the relevance of CD25 (IL-2 receptor α) in the process. We injected IL-2 intradermally into WT mice and observed increases in immune cell subsets in the skin with preferential increases in frequencies of IL-4- and IL-13-producing group 2 innate lymphoid cells and IL-17-producing dermal γδ T cells. This overall led to a shift toward type 2/type 17 immune responses. In addition, using a novel topical genetic deletion approach, we reduced CD25 on skin, specifically on all cutaneous cells, and found that IL-2-dependent effects were reduced, hinting that CD25 - at least partly - induces this skin inflammation. Reduction of CD25 specifically on skin Tregs further augmented IL-2-induced immune cell infiltration, hinting that CD25 on skin Tregs is crucial to restrain IL-2-induced inflammation. Overall, our data support that innate lymphoid immune cells are key cells inducing side effects during IL-2 therapy and underline the significance of CD25 in this process.
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.
Interleukin-2-induced skin inflammation. · full record | OpenQuestion