DNASE1L3 Deficiency, New Phenotypes and Evidence for a Transient Type I Interferon Signaling Article Swipe
Maud Tusseau
,
Ema Lovšin
,
Charlotte Samaille
,
Rémi Pescarmona
,
Maria Cristina Maggio
,
Velma Selmanović
,
Maruša Debeljak
,
Angélique Dachy
,
Alexandre Janin
,
Louis Januel
,
Anne‐Laure Mathieu
,
Jean Baptiste Gibier
,
Emilie Chopin
,
Isabelle Rouvet
,
David Gonçalves
,
Nicole Fabien
,
Gillian Rice
,
Audrey Labalme
,
Paola Romagnani
,
Gaëtan Lesca
,
Thierry Walzer
,
Sébastien Viel
,
Magali Perret
,
Yannick Crow
,
Tadej Avčin
,
Rolando Cimaz
,
Alexandre Bélot
·
YOU?
·
· 2021
· Open Access
·
· DOI: https://doi.org/10.21203/rs.3.rs-502604/v1
YOU?
·
· 2021
· Open Access
·
· DOI: https://doi.org/10.21203/rs.3.rs-502604/v1
Deoxyribonuclease 1 like 3 (DNASE1L3) is a secreted enzyme that has been shown to digest the extracellular chromatin derived from apoptotic bodies, and DNASE1L3 pathogenic variants have been associated to a lupus phenotype. It is unclear whether interferon signaling is sustained in DNASE1L3 deficiency in humans. Here we report four new patients carrying biallelic DNASE1L3 pathogenic variations, including two previously unreported mutations. Disease in one patient was characterized by lupus nephritis and skin lesions, while two others exhibited hypocomplementemic urticarial vasculitis syndrome. The fourth patient presented with early-onset inflammatory bowel disease. To explore whether or not the interferon cascade was strongly and sustainably induced, Interferon stimulated genes (ISGs) expression was assessed for each patient. Contrary to canonical type-I interferonopathies, we noticed a transient increase of ISGs in blood, which reverted to normal with disease remission. Reviewing previous reports, DNASE1L3-related disease appears to carry a significant risk of lupus nephritis and a poor outcome together with the presence of anti-neutrophil cytoplasmic antibodies (ANCA). DNASE1L3 deficiency may share the pathogenesis with C1q deficiency by affecting efferocytosis, and this report suggests that interferon production is not directly driven by DNASE1L3 pathogenic variants.
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Metadata
- Type
- preprint
- Language
- en
- Landing Page
- https://doi.org/10.21203/rs.3.rs-502604/v1
- https://www.researchsquare.com/article/rs-502604/latest.pdf
- OA Status
- green
- References
- 21
- Related Works
- 10
- OpenAlex ID
- https://openalex.org/W3165289535
All OpenAlex metadata
Raw OpenAlex JSON
- OpenAlex ID
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https://openalex.org/W3165289535Canonical identifier for this work in OpenAlex
- DOI
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https://doi.org/10.21203/rs.3.rs-502604/v1Digital Object Identifier
- Title
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DNASE1L3 Deficiency, New Phenotypes and Evidence for a Transient Type I Interferon SignalingWork title
- Type
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preprintOpenAlex work type
- Language
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enPrimary language
- Publication year
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2021Year of publication
- Publication date
-
2021-05-24Full publication date if available
- Authors
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Maud Tusseau, Ema Lovšin, Charlotte Samaille, Rémi Pescarmona, Maria Cristina Maggio, Velma Selmanović, Maruša Debeljak, Angélique Dachy, Alexandre Janin, Louis Januel, Anne‐Laure Mathieu, Jean Baptiste Gibier, Emilie Chopin, Isabelle Rouvet, David Gonçalves, Nicole Fabien, Gillian Rice, Audrey Labalme, Paola Romagnani, Gaëtan Lesca, Thierry Walzer, Sébastien Viel, Magali Perret, Yannick Crow, Tadej Avčin, Rolando Cimaz, Alexandre BélotList of authors in order
- Landing page
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https://doi.org/10.21203/rs.3.rs-502604/v1Publisher landing page
- PDF URL
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https://www.researchsquare.com/article/rs-502604/latest.pdfDirect link to full text PDF
- Open access
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YesWhether a free full text is available
- OA status
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greenOpen access status per OpenAlex
- OA URL
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https://www.researchsquare.com/article/rs-502604/latest.pdfDirect OA link when available
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Phenotype, Interferon, Transient (computer programming), Signal transduction, Biology, Cell biology, Immunology, Genetics, Computer science, Gene, Operating systemTop concepts (fields/topics) attached by OpenAlex
- Cited by
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0Total citation count in OpenAlex
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21Number of works referenced by this work
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10Other works algorithmically related by OpenAlex
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