ReviewSeminars in respiratory and critical care medicine2025
Immunopathogenesis of Sarcoidosis.
Review in Seminars in respiratory and critical care medicine, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 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
3 citing papers in PubMed.
- Medico-legal difficulties in a death due to delayed traumatic rupture of massive sarcoid spleen with rivaroxaban therapy.Forensic science, medicine, and pathology · 2026Article
- Quality of Life in Sarcoidosis.Diagnostics (Basel, Switzerland) · 2026Review
- Uncovering Sex and Gender Differences in Sarcoidosis: A Systematic Review of Current Evidence.Journal of personalized medicine · 2026Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Sarcoidosis is a granulomatous disease of unknown cause, triggered by an unidentified antigen. Although classically considered a T cell-mediated disorder with an IFN-γ signature driven by Th1, Th17, and Th17.1 cells, its pathogenesis reflects dysregulated crosstalk between innate and adaptive immunity. Granulomas form through macrophage differentiation at the core, fueled by aberrantly programmed monocytes and sustained by persistent antigen presentation to T cells. Hyperactive macrophages drive excessive peripheral cell recruitment, while dysregulated T cell responses promote T cell expansion, impaired effector regulation, and eventual exhaustion. Deficient regulatory pathways fail to counterbalance this activation, creating a perpetuating inflammatory loop that underlies disease persistence and fibrotic progression. This review integrates up-to-date transcriptomic and biological data to define the cellular and molecular mechanisms that initiate, sustain, and dysregulate immune responses in sarcoidosis.
Indexed as
Identifiers
What Socratic 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 Socratic graph.