Evidence map›Paper›PMID 42774716›Full record

ReviewFrontiers in immunology2026

Lymphocyte signal transduction defects in cutaneous sarcoidosis and implications for treatment.

Julia Lunt, Adarsh Shidhaye, Christine Fasana, Meredith Morgan, William M Schmidt, Daniel L Lee, Sherry Chen, Katherine E McCain, Christine Schammel, Steven E Fiester and 2 more

Abstract readReview
In one paragraph

Review in Frontiers in immunology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing 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

0 citing papers in PubMed.

No citing paper in PubMed yet.

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

12 authors.

Julia LuntDepartment of Biomedical Sciences, University of South Carolina School of Medicine Greenville, Greenville, SC, United States.
Adarsh ShidhayeDepartment of Biomedical Sciences, University of South Carolina School of Medicine Greenville, Greenville, SC, United States.
Christine FasanaDepartment of Biomedical Sciences, University of South Carolina School of Medicine Greenville, Greenville, SC, United States.
Meredith MorganDepartment of Biomedical Sciences, University of South Carolina School of Medicine Greenville, Greenville, SC, United States.
William M SchmidtDepartment of Biomedical Sciences, University of South Carolina School of Medicine Greenville, Greenville, SC, United States.
Daniel L LeeDepartment of Biomedical Sciences, University of South Carolina School of Medicine Greenville, Greenville, SC, United States.
Sherry ChenDepartment of Biomedical Sciences, University of South Carolina School of Medicine Greenville, Greenville, SC, United States.
Katherine E McCainDepartment of Biological Sciences, University of South Carolina, Columbia, SC, United States.
Christine SchammelDepartment of Pathology, Prisma Health, Greenville, SC, United States.
Steven E FiesterPathology Associates and Consultants, Greenville, SC, United States.
Sergio ArceDepartment of Biomedical Sciences, University of South Carolina School of Medicine Greenville, Greenville, SC, United States.
Jennifer T GrierDepartment of Biomedical Sciences, University of South Carolina School of Medicine Greenville, Greenville, SC, United States.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Sarcoidosis is a multiorgan immunological disease characterized by an exaggerated inflammatory response leading to non-caseating granuloma formation. Cutaneous sarcoidosis lesions serve as an accessible site for biopsy that can assist with earlier identification and treatment of sarcoid disease. This review synthesizes recent advances in the understanding of cutaneous sarcoidosis immunopathogenesis, with a focus on lymphocyte signaling, and describes the therapeutic implications of this immune dysregulation. While it is known that Th1 and Th17 cell subsets contribute to general non-caseating granuloma formation, recent studies identify Th17.1 cells as the predominant producers of IFN-γ, challenging classical paradigms. Th2 polarization and elevated thymus and activation-regulated chemokine (TARC) levels, along with regulatory T cell dysfunction and PD-1 overexpression, contribute to chronic inflammation and fibrosis in the cutaneous sarcoidosis disease state. The JAK/STAT pathway is notably upregulated in cutaneous sarcoid granulomas, and JAK inhibitors have demonstrated promising efficacy as an avenue for treatment. Additional immune mechanisms at play in cutaneous sarcoidosis include mTOR and TLR dysregulation as well as B-cell dysfunction. Infectious triggers and DNA polymorphisms associated with genetic susceptibility further support the multifactorial nature of cutaneous sarcoidosis. Based on current literature and clinical guidelines, we propose treatment options for cutaneous sarcoidosis which target dysregulated aspects of the immune response. While prednisone and corticotropin gel remain the only FDA-approved therapies for cutaneous sarcoidosis, improved understanding of sarcoidosis signaling may lead to promising new therapeutic approaches. With the growing understanding of lymphocyte signaling defects in cutaneous sarcoidosis, physicians will be better equipped to identify and treat the underlying mechanisms of this disease.

Indexed as

LymphocytesSarcoidosisSignal TransductionSkin DiseasesAnimalsHumanscutaneous sarcoidosiscutaneous sarcoidosis treatmentgranulomasgranulomatous diseasenon-caseating granulomassarcoidosis

Identifiers

PMID42774716
PMCPMC13594530

What OpenQuestion holds

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Registered trials

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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.