Evidence map›Paper›PMID 33572487›Full record

ReviewBiomolecules2021

The Role of Interferons in the Pathogenesis of Sjögren's Syndrome and Future Therapeutic Perspectives.

Nicoletta Del Papa, Antonina Minniti, Maurizio Lorini, Vincenzo Carbonelli, Wanda Maglione, Francesca Pignataro, Nicola Montano, Roberto Caporali, Claudio Vitali

Open access · goldAbstract readReview
In one paragraph

Review in Biomolecules, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
42citing papers in PubMed, 1 pooled it
4.7field-weighted citation impact, top 4% 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

42 citing papers in PubMed, 1 synthesis or guideline pooled it, 61 citations in OpenAlex.

  1. Guideline
  2. Review
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  5. Review
  6. Article
  7. Article
  8. Review
  9. Review
  10. Article
  11. Review
  12. Review
  13. mRNA Isoforms and Variants in Health and Disease.International journal of molecular sciences · 2025
    Review
  14. Sjogren's Disease and Elevated Cardiovascular Risk: Mechanisms and Treatment.Journal of cardiovascular development and disease · 2025
    Review
  15. Article
  16. Article
  17. Article
  18. Article
  19. Article
  20. 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

9 authors at 3 institutions in 1 country.

Nicoletta Del PapaDepartment of Rheumatology, ASST G. Pini-CTO, 20122 Milano, Italy.ORCID 0000-0003-1549-8852
Antonina MinnitiDepartment of Rheumatology, ASST G. Pini-CTO, 20122 Milano, Italy.
Maurizio LoriniDepartment of Clinical Sciences and Community Health, Ca' Granda IRCCS Foundation, Ospedale Maggiore Policlinico, Università degli Studi di Milano, 20122 Milano, Italy.
Vincenzo CarbonelliDepartment of Clinical Sciences and Community Health, Ca' Granda IRCCS Foundation, Ospedale Maggiore Policlinico, Università degli Studi di Milano, 20122 Milano, Italy.
Wanda MaglioneDepartment of Rheumatology, ASST G. Pini-CTO, 20122 Milano, Italy.
Francesca PignataroDepartment of Rheumatology, ASST G. Pini-CTO, 20122 Milano, Italy.
Nicola MontanoDepartment of Clinical Sciences and Community Health, Ca' Granda IRCCS Foundation, Ospedale Maggiore Policlinico, Università degli Studi di Milano, 20122 Milano, Italy.ORCID 0000-0001-9206-0075
Roberto CaporaliDepartment of Rheumatology, ASST G. Pini-CTO, 20122 Milano, Italy.
Claudio VitaliMater Domini Humanitas Hospital, Rheumatology Outpatient Clinics, 21053 Castellanza, Italy.
Istituto Ortopedico Gaetano Pini · ITUniversity of Milan · ITHumanitas Mater Domini · IT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

There is a great deal of evidence pointing to interferons (IFNs) as being key cytokines in the pathogenesis of different systemic autoimmune diseases, including primary Sjögren's syndrome (pSS). In this disease, a large number of studies have shown that an overexpression of type I IFN, the 'so-called' type I IFN signature, is present in peripheral blood mononuclear cells, and that this finding is associated with the development of systemic extra-glandular manifestations, and a substantial production of autoantibodies and inflammatory cytokines. In contrast, the absence or a milder expression of type I IFN signature and low level of inflammatory cytokines characterizes patients with a different clinical phenotype, where the disease is limited to glandular involvement and often marked by the presence of widespread pain and depression. The role of type II (IFNγ) in this subset of pSS patients, together with the potentially related activation of completely different immunological and metabolic pathways, are emerging issues. Expression of both types of IFNs has also been shown in target tissues, namely in minor salivary glands where a predominance of type II IFN signature appeared to have a certain association with the development of lymphoma. In view of the role played by IFN overexpression in the development and progression of pSS, inhibition or modulation of IFN signaling has been regarded as a potential target for the therapeutic approach. A number of therapeutic compounds with variable mechanisms of action have been tested or are under consideration for the treatment of patients with pSS.

Indexed as

AnimalsHumansInterferon-gammaInterferon Type ISalivary GlandsSignal TransductionSjogren's SyndromeInterferon-gammaInterferon Type ISjögren’s syndrometarget therapiestype II interferontype I interferon

Identifiers

PMID33572487
PMCPMC7916411
OpenAlexW3126281925

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.