Evidence map›Paper›PMID 22631445›Full record

ReviewPhotochemistry and photobiology

Inflammasome activation of IL-1 family mediators in response to cutaneous photodamage.

Tahseen H Nasti, Laura Timares

Abstract readReview
In one paragraph

Review in Photochemistry and photobiology. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 43 papers.

0numbers the graph read from it
0cells of the map it votes in
43citing papers in PubMed
3.6field-weighted citation impact, top 6% 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

43 citing papers in PubMed, 100 citations in OpenAlex.

  1. Trial
  2. Trial
  3. Trial
  4. Review
  5. From Reshaped Metabolome to Repaired Skin: FermentedAntioxidants (Basel, Switzerland) · 2025
    Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. UVB-Induced Secretion of IL-1BioMed research international · 2022
    Article
  12. Review
  13. The Immunogenetics of Melanoma.Advances in experimental medicine and biology · 2022
    Article
  14. Article
  15. Review
  16. Article
  17. Review
  18. Review
  19. Article
  20. Article
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

2 authors at 1 institution in 1 country.

Tahseen H NastiDepartment of Dermatology, University of Alabama at Birmingham, Birmingham, AL, USA.
Laura Timares
University of Alabama at Birmingham · US

Funding

ROS Modulation of Innate and Adaptive Immunity in RAP30AR048311 · NIAMS · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI MOUNTZ, JOHN D · 2001 to 2017
$9.5M
UAB Skin Diseases Research CenterP30AR050948 · NIAMS · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI ELMETS, CRAIG A · 2004 to 2013
$5.5M
Apoptosis-Resistant Langerhans CellsR01AI050150 · NIAID · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI TIMARES, LAURA · 2002 to 2004
$702k
Bid Regulation of Cutaneous Photodamage ResponsesR21AR055252 · NIAMS · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI TIMARES, LAURA · 2009 to 2010
$360k
NIAID NIH HHS R01 AI050150NIAMS NIH HHS P30 AR048311NIAMS NIH HHS P30 AR050948NIAMS NIH HHS P30 AR-05-0948-05NIAMS NIH HHS R21 AR055252NIAMS NIH HHS R21AR055252
6 · The paper itself

Abstract

Although keratinocytes are relatively resistant to ultraviolet radiation (UVR) induced damage, repeated UVR exposure result in accumulated DNA mutations that can lead to epidermal malignancies. Keratinocytes play a central role in elaborating innate responses that lead to inflammation and influence the generation of adaptive immune responses in skin. Apart from the minor cellular constituents of the epidermis, specifically Langerhans cells and melanocytes, keratinocytes are the major source of cytokines. UVR exposure stimulates keratinocytes to secrete abundant pro-inflammatory IL-1-family proteins, IL-1α, IL-1β, IL-18, and IL-33. Normal skin contains only low levels of inactive precursor forms of IL-1β and IL-18, which require caspase 1-mediated proteolysis for their maturation and secretion. However, caspase-1 activation is not constitutive, but dependents on the UV-induced formation of an active inflammasome complex. IL-1 family cytokines can induce a secondary cascade of mediators and cytokines from keratinocytes and other cells resulting in wide range of innate processes including infiltration of inflammatory leukocytes, induction of immunosuppression, DNA repair or apoptosis. Thus, the ability of keratinocytes to produce a wide repertoire of proinflammatory cytokines can influence the immune response locally as well as systematically, and alter the host response to photodamaged cells. We will highlight differential roles played by each IL-1 family molecule generated by UV-damaged keratinocytes, and reveal their complementary influences in modulating acute inflammatory and immunological events that follow cutaneous UV exposure.

Indexed as

ApoptosisDNADNA RepairEpidermal CellsEpidermisHumansImmunity, InnateInflammasomesInflammationInterleukin-18Interleukin-1alphaInterleukin-1betaInterleukin-33InterleukinsKeratinocytesSignal TransductionDNAIL33 protein, humanInflammasomesInterleukin-18Interleukin-1alphaInterleukin-1betaInterleukin-33Interleukins

Identifiers

PMID22631445
PMCPMC3435462
OpenAlexW1557720945

What OpenQuestion holds

Textmetadata
LicenceTDM
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.