Evidence map›Paper›PMID 36865257›Full record

ArticleResearch square2023

Dysregulated CD38 expression in blood and skin immune cells of patients with hidradenitis suppurativa.

Qing-Sheng Mi, Peter Dimitrion, Iltefat Hamzavi, Congcong Yin, Ian Loveless, Jugmohit Toor, Kalpana Subedi, Richard Huggins, Namir Khalasawi, Indra Adrianto and 9 more

Open access · greenAbstract readPreprint
In one paragraph

Article in Research square, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
–field-weighted citation impact
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

1 citing paper in PubMed, 2 citations in OpenAlex.

  1. Review
4 · The record

Corrections and comments

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

19 authors at 4 institutions in 1 country.

Qing-Sheng MiHenry Ford Health.ORCID 0000-0002-1411-6827
Peter DimitrionHenry Ford Health.
Iltefat HamzaviHenry Ford Heatlh.
Congcong YinHenry Ford Health System.
Ian LovelessHenry Ford Health System.ORCID 0000-0003-4645-6559
Jugmohit ToorHenry Ford Health.
Kalpana SubediHenry Ford Health System.
Richard HugginsHenry Ford Health.
Namir KhalasawiHenry Ford Health.
Indra AdriantoHenry Ford Health System.ORCID 0000-0002-9973-3057
Jesse VeenstraHenry Ford Health.
Gautham VellaichamyHenry Ford Health.
Aakash HansHenry Ford Health.
Steven DaveluyWayne State University School of Medicine.
Mohammad AtharUniversity of Alabama-Birmingham School of Medicine.
Wilson LiaoUniversity of California-San Francisco School of Medicine.
Henry LimHenry Ford Health.
David OzogHenry Ford Health.
Li ZhouHenry Ford Health System.
Henry Ford Health System · USUniversity of Alabama at Birmingham · USUniversity of California, San Francisco · USWayne State University · US

Funding

Using whole-exome sequencing to uncover key genetic variants related to Hidradenitis Suppurativa risk in African American and Hispanic population.R01AR078688 · NIAMS · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI LIAO, WILSON, MI, QING-SHENG · 2021 to 2025
$4.1M
Genetic risk of hidradenitis suppurativa in African AmericansR21AR079089 · NIAMS · HENRY FORD HEALTH SYSTEM · PI ADRIANTO, INDRA, MI, QING-SHENG · 2022 to 2023
$520k
NIAMS NIH HHS R01 AR078688NIAMS NIH HHS R21 AR079089
6 · The paper itself

Abstract

Hidradenitis suppurativa (HS) is a multifactorial, inflammatory skin disease. Increased systemic inflammatory comorbidities and serum cytokines highlight systemic inflammation as a feature of HS. However, the specific immune cell subsets contributing to systemic and cutaneous inflammation have not been resolved. Here, we generated whole-blood immunomes by mass cytometry. We performed a meta-analysis of RNA-seq data, immunohistochemistry, and imaging mass cytometry to characterize the immunological landscape of skin lesions and perilesions from patients with HS. Blood from patients with HS exhibited lower frequencies of natural killer cells, dendritic cells, and classical (CD14+CD16-) and nonclassical (CD14-CD16+) monocytes, as well as higher frequencies of Th17 cells and intermediate (CD14+CD16+) monocytes than blood from healthy controls. Classical and intermediate monocytes from patients with HS had increased expression of skin-homing chemokine receptors. Furthermore, we identified a CD38+ intermediate monocyte subpopulation that was more abundant in the immunome of blood from patients with HS. Meta-analysis of RNA-seq data found higher CD38 expression in lesional HS skin than in perilesional skin, and markers of classical monocyte infiltration. Imaging mass cytometry showed that CD38+ classical monocytes and CD38+ monocyte-derived macrophages were more abundant in lesional HS skin. Overall, we report targeting CD38 may be worth pursuing in clinical trials.

Identifiers

PMID36865257
PMCPMC9980201
OpenAlexW4321770217

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

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.