Definition and research guide
This page combines a MeSH definition, publication statistics and selected research abstracts. It is a starting point for reading the literature, not a medical textbook or a systematic evidence review.
Content available: 4 complete abstracts (701 words), 10 references. Full article text is not stored or reproduced here; follow the PMID, DOI or PMC links to read the original sources and their access terms.
Definition
An idiopathic systemic inflammatory granulomatous disorder comprised of epithelioid and multinucleated giant cells with little necrosis. It usually invades the lungs with fibrosis and may also involve lymph nodes, skin, liver, spleen, eyes, phalangeal bones, and parotid glands.
Definition: NLM Medical Subject Headings (MeSH) scope note (Public domain (U.S. National Library of Medicine); attribution requested). View the MeSH record.
Also known as: Sarcoidoses; Schaumann's Syndrome; Schaumann's Syndromes; Syndrome, Schaumann's; Besnier-Boeck-Schaumann Syndrome; Besnier Boeck Schaumann Syndrome; Syndrome, Besnier-Boeck-Schaumann; Boeck Disease.
Where it fits in the MeSH classification
- Broader topics
- Lymphoproliferative Disorders; Hypersensitivity, Delayed
- Narrower topics
- Sarcoidosis, Pulmonary; Uveoparotid Fever
- See also
- Kveim Test
Research landscape
PubMed indexes 28,417 records tagged with the MeSH heading “Sarcoidosis” (counts retrieved 2026-10-29). 3,362 of them (11.8%) were published from 2020 onward, and the busiest period so far is through 1999 with 15,112 records.
Reviews account for 3,537 records (12.4%) and meta-analyses for 93. Randomized controlled trials number 94 (0.3%) as a share of all records on the topic. Randomized trials make up only a small share of this literature, so much of what is known comes from laboratory, observational or descriptive work.
Show the data
| Period | Records |
|---|---|
| through 1999 | 15,112 |
| 2000-2009 | 4,404 |
| 2010-2019 | 5,539 |
| 2020 onward | 3,362 |
Publication-type chart data
| Type | Records | Share |
|---|---|---|
| Reviews | 3,537 | 12.4% |
| Meta-analyses | 93 | 0.3% |
| Randomized controlled trials | 94 | 0.3% |
Method: PubMed query "Sarcoidosis"[MeSH Terms] with publication-type and date filters, retrieved 2026-10-29.
Reading the evidence in immunology
Immune responses are studied in model organisms, in cells from donors and in patients, and the same pathway can behave differently across these settings. Mouse immune systems differ from human ones in important ways, and blood measurements may not reflect what happens in tissues. Clinical conclusions about immune-mediated disease or immunotherapy come mainly from controlled trials and long-term cohorts. Check the species and tissue studied, whether markers were linked to outcomes patients notice, and the follow-up time.
Evidence from open-access studies
These open-access studies come from PubMed’s best-match results for this heading (papers whose main topic it is), ranked here by citation count, with one recent addition. Each abstract is reproduced in full under its recorded open licence so that you can read the authors’ own words. They illustrate the literature; they are not a systematic summary of it. Citation counts measure attention, not reliability or clinical benefit.
| Study / authors | Year | Source label / design | Europe PMC citations | Licence / source |
|---|---|---|---|---|
| Meta-analysis of [18F]FDG-PET/CT in pulmonary sarcoidosis | 2025 | Meta-analysis Design not recorded in structured metadata | 24 | cc by PMID 39044038 · DOI · PMC11913913 |
| Sarcoidosis: molecular mechanisms and therapeutic strategies | 2025 | Review article Design not recorded in structured metadata | 23 | cc by PMID 39904950 · DOI · PMC11794924 |
| Sarcoidosis: a general overview | 2024 | Review article Design not recorded in structured metadata | 21 | cc by PMID 39135190 · DOI · PMC13488721 |
| Legumain Restrains Granuloma Formation by Inhibiting mTORC1/STAT1-Mediated M1 Macrophage Polarization in Sarcoidosis | 2026 | Research article Design not recorded in structured metadata | 3 | cc by PMID 41933939 · DOI · PMC13271614 |
Meta-analysis of [18F]FDG-PET/CT in pulmonary sarcoidosis [1]
Abstract reading summary — source excerpts
- Opening excerpt
- Background18F-Fluorodeoxyglucose (FDG) PET/CT is emerging as a tool in the diagnosis and evaluation of pulmonary sarcoidosis, however, there is limited consensus regarding its diagnostic performance and prognostic value.
- Closing excerpt
- Reduction in SUVmax correlated with an improvement in functional vital capacity, Diffusion Capacity of the Lungs for Carbon Monoxide, and subjective health scoring systems.
- Interpretation limits
- Verbatim excerpts from the authors’ abstract; the closing excerpt may describe a finding, limitation or recommendation. Design, population, effect size and uncertainty have not been independently extracted or appraised. Read the complete abstract and linked paper before interpreting the findings.
Read complete abstract (240 words)
Background18F-Fluorodeoxyglucose (FDG) PET/CT is emerging as a tool in the diagnosis and evaluation of pulmonary sarcoidosis, however, there is limited consensus regarding its diagnostic performance and prognostic value.MethodA meta-analysis was conducted with PubMed, Science Direct, MEDLINE, Scopus, and CENTRAL databases searched up to and including September 2023. 1355 studies were screened, with seventeen (n = 708 patients) suitable based on their assessment of the diagnostic performance or prognostic value of FDG-PET/CT. Study quality was assessed using the QUADAS-2 tool. Forest plots of pooled sensitivity and specificity were generated to assess diagnostic performance. Pooled changes in SUVmax were correlated with changes in pulmonary function tests (PFT).ResultsFDG-PET/CT in diagnosing suspected pulmonary sarcoidosis (six studies, n = 400) had a pooled sensitivity of 0.971 (95%CI 0.909-1.000, p = ConclusionIn cases of suspected pulmonary sarcoidosis, FDG-PET/CT demonstrated good diagnostic performance and correlated with functional health scores. FDG-PET/CT may help to guide immunosuppression in cases of complex sarcoidosis or where treatment rationalisation is needed.Clinical relevance statementFDG-PET/CT has demonstrated a high diagnostic performance in the evaluation of suspected pulmonary sarcoidosis with radiologically assessed disease activity correlating strongly with clinically derived pulmonary function tests.Key pointsIn diagnosing pulmonary sarcoidosis, FDG-PET/CT had a sensitivity and specificity of 0.971 and 0.873, respectively. Disease activity, as determined by SUVmax, reduced following treatment in all the included studies. Reduction in SUVmax correlated with an improvement in functional vital capacity, Diffusion Capacity of the Lungs for Carbon Monoxide, and subjective health scoring systems.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 39044038 · DOI · PMC11913913
Sarcoidosis: molecular mechanisms and therapeutic strategies [2]
Abstract reading summary — source excerpts
- Opening excerpt
- Sarcoidosis, a multisystemic granulomatous disease with unknown etiology, is characterized by formation of noncaseating granulomas, which can affect all organs.
- Closing excerpt
- This review outlines recent advancements in the molecular mechanisms and therapeutic strategies for the sarcoidosis.
- Interpretation limits
- Verbatim excerpts from the authors’ abstract; the closing excerpt may describe a finding, limitation or recommendation. Design, population, effect size and uncertainty have not been independently extracted or appraised. Read the complete abstract and linked paper before interpreting the findings.
Read complete abstract (210 words)
Sarcoidosis, a multisystemic granulomatous disease with unknown etiology, is characterized by formation of noncaseating granulomas, which can affect all organs. Recent studies have made outstanding achievement in understanding the pathology, etiology, genetics, and immune dysregulation involved in granuloma formation of sarcoidosis. Antigen stimulation in genetically predisposed individuals enhances the phagocytic activity of antigen-presenting cells, including macrophages and dendritic cells. CD4 + T cells initiate dysregulated immune responses and secrete significant quantities of inflammatory cytokines, including interleukin (IL)-2 and interferon-gamma (IFN-γ), which play a crucial role in modulating the aggregation and fusion of macrophages to form granulomas. The current therapeutic strategies focus on blocking the formation and spread of granulomas to protect organ function and alleviate symptoms. The efficacy of traditional treatments, such as glucocorticoids and immunosuppressants, has been confirmed in the management of sarcoidosis. Promising therapeutic agents encompass inhibitors of cytokines, like those targeting tumor necrosis factor (TNF)-α, as well as inhibitors of signaling pathways, such as Janus kinase (JAK) inhibitors, which exhibit favorable prospects for application. Although there has been progress in the identification of biomarkers for the diagnosis, prognosis, activity and severity of sarcoidosis, specific and sensitive biomarkers have yet to be identified. This review outlines recent advancements in the molecular mechanisms and therapeutic strategies for the sarcoidosis.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 39904950 · DOI · PMC11794924
Sarcoidosis: a general overview [3]
Abstract reading summary — source excerpts
- Opening excerpt
- Sarcoidosis is a systemic inflammatory disease of unknown origin, which consists of the formation of multiple sterile noncaseating granulomas.
- Closing excerpt
- In this article, we review current concepts about sarcoidosis in an overview, focusing on recognition and treatment of its major clinical phenotypes.
- Interpretation limits
- Verbatim excerpts from the authors’ abstract; the closing excerpt may describe a finding, limitation or recommendation. Design, population, effect size and uncertainty have not been independently extracted or appraised. Read the complete abstract and linked paper before interpreting the findings.
Read complete abstract (87 words)
Sarcoidosis is a systemic inflammatory disease of unknown origin, which consists of the formation of multiple sterile noncaseating granulomas. Inhaled antigens are believed to initiate disease in prone individuals, considering that almost all patients present pulmonary or mediastinal lymph node disease. Extrapulmonary manifestations are common and diverse: practically any organ system can be affected, and treatment can range from simple watchful waiting to intense immunosuppression. In this article, we review current concepts about sarcoidosis in an overview, focusing on recognition and treatment of its major clinical phenotypes.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 39135190 · DOI · PMC13488721
Legumain Restrains Granuloma Formation by Inhibiting mTORC1/STAT1-Mediated M1 Macrophage Polarization in Sarcoidosis [4]
Abstract reading summary — source excerpts
- Opening excerpt
- Sarcoidosis is a systemic granulomatous disease that has limited treatment options.
- Closing excerpt
- Therefore, LGMN supplementation may be a promising therapeutic strategy for sarcoidosis.
- Interpretation limits
- Verbatim excerpts from the authors’ abstract; the closing excerpt may describe a finding, limitation or recommendation. Design, population, effect size and uncertainty have not been independently extracted or appraised. Read the complete abstract and linked paper before interpreting the findings.
Read complete abstract (164 words)
Sarcoidosis is a systemic granulomatous disease that has limited treatment options. Emerging evidence suggests that macrophages are essential for sarcoid granuloma initiation. Legumain (LGMN), a cysteine protease, regulates macrophage polarization in various cancers. However, its involvement in sarcoid granuloma formation remains elusive. Herein, LGMN is upregulated in macrophages within sarcoid-like granulomas. Genetic deletion of Lgmn exacerbates granulomatous inflammation in a Propionibacterium acnes (P. acnes)-induced mouse model, accompanied by increased M1 macrophage polarization. Mechanistically, LGMN binds to integrin αvβ3 on the macrophage surface and restrains M1 polarization by inhibiting the mechanistic target of rapamycin complex 1 (mTORC1)/signal transducer and activator of transcription 1 (STAT1) pathway. Furthermore, intratracheal administration of lipid nanoparticles carrying Lgmn plasmid DNA effectively alleviates granuloma formation induced by P. acnes or trehalose 6,6'-dimycolate, concomitant with decreased mTORC1/STAT1 activation and M1 polarization. These findings reveal the pivotal role of LGMN in restraining sarcoid granulomatous inflammation through suppression of mTORC1/STAT1-driven M1 macrophage polarization. Therefore, LGMN supplementation may be a promising therapeutic strategy for sarcoidosis.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 41933939 · DOI · PMC13271614
Key reviews and meta-analyses
The most cited review-type papers among PubMed’s best-match results for this heading, listed with bibliographic details only. Follow the links for the full text and access terms.
- Research article Clinical features, treatment and outcome in neurosarcoidosis: systematic review and meta-analysis [5]
- Research article Diagnosis and Management of Cardiac Sarcoidosis: A Scientific Statement From the American Heart Association [6]
- Research article Neurosarcoidosis: Pathophysiology, Diagnosis, and Treatment [7]
- Research article Diagnosis and Treatment of Pulmonary Sarcoidosis: A Review [8]
- Research article Pyroptosis in inflammation-related respiratory disease [9]
- Research article Sarcoidosis and cancer risk: systematic review and meta-analysis of observational studies [10]
References
- Donnelly R, McDermott M, McManus G, Franciosi AN, Keane MP, McGrath EE, et al.. Meta-analysis of [18F]FDG-PET/CT in pulmonary sarcoidosis. . 2025. PMID 39044038 · DOI · PMC11913913
- Xu D, Tao X, Fan Y, Teng Y. Sarcoidosis: molecular mechanisms and therapeutic strategies. . 2025. PMID 39904950 · DOI · PMC11794924
- Neves FS, Pereira IA, Sztajnbok F, Neto NSR. Sarcoidosis: a general overview. . 2024. PMID 39135190 · DOI · PMC13488721
- Liu M, Han Y, Xie B, Zhu L, Xu W, Han Y, et al.. Legumain Restrains Granuloma Formation by Inhibiting mTORC1/STAT1-Mediated M1 Macrophage Polarization in Sarcoidosis. . 2026. PMID 41933939 · DOI · PMC13271614
- Fritz D, van de Beek D, Brouwer MC. Clinical features, treatment and outcome in neurosarcoidosis: systematic review and meta-analysis. BMC Neurol. 2016. PMID 27846819 · DOI · PMC5109654
- Cheng RK, Kittleson MM, Beavers CJ, Birnie DH, Blankstein R, Bravo PE, et al.. Diagnosis and Management of Cardiac Sarcoidosis: A Scientific Statement From the American Heart Association. Circulation. 2024. PMID 38634276 · DOI
- Bradshaw MJ, Pawate S, Koth LL, Cho TA, Gelfand JM. Neurosarcoidosis: Pathophysiology, Diagnosis, and Treatment. Neurol Neuroimmunol Neuroinflamm. 2021. PMID 34607912 · DOI · PMC8495503
- Belperio JA, Shaikh F, Abtin FG, Fishbein MC, Weigt SS, Saggar R, et al.. Diagnosis and Treatment of Pulmonary Sarcoidosis: A Review. JAMA. 2022. PMID 35230389 · DOI
- Feng Y, Li M, Yangzhong X, Zhang X, Zu A, Hou Y, et al.. Pyroptosis in inflammation-related respiratory disease. J Physiol Biochem. 2022. PMID 35819638 · DOI · PMC9684248
- Bonifazi M, Bravi F, Gasparini S, La Vecchia C, Gabrielli A, Wells AU, et al.. Sarcoidosis and cancer risk: systematic review and meta-analysis of observational studies. Chest. 2015. PMID 25340385 · DOI
About this article
- Sources
- NLM Medical Subject Headings (definition, synonyms); NCBI PubMed (counts, identifiers); Europe PMC (open-access abstracts and citation counts).
- Verification
- Every reference was resolved against PubMed on 2026-10-31; title, year and DOI matched.
- Review state
- automated source verified; no human expert review has been recorded yet.
- Version
- 1, last updated 2026-10-29.
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Evidence strength
EvidenceHelix's computed view of the study designs behind this topic: how common meta-analyses, randomized trials and reviews are, how recent the literature is, and a plain-language reading. It describes the design mix of the literature. It is not a quality appraisal of any study, and it is not medical advice.