Secretome screening reveals immunomodulating functions of IFNα-7, PAP and GDF-7 on regulatory T-cells.


Journal

Scientific reports
ISSN: 2045-2322
Titre abrégé: Sci Rep
Pays: England
ID NLM: 101563288

Informations de publication

Date de publication:
18 08 2021
Historique:
received: 20 01 2021
accepted: 05 08 2021
entrez: 19 8 2021
pubmed: 20 8 2021
medline: 12 11 2021
Statut: epublish

Résumé

Regulatory T cells (Tregs) are the key cells regulating peripheral autoreactive T lymphocytes. Tregs exert their function by suppressing effector T cells. Tregs have been shown to play essential roles in the control of a variety of physiological and pathological immune responses. However, Tregs are unstable and can lose the expression of FOXP3 and suppressive functions as a consequence of outer stimuli. Available literature suggests that secreted proteins regulate Treg functional states, such as differentiation, proliferation and suppressive function. Identification of secreted proteins that affect Treg cell function are highly interesting for both therapeutic and diagnostic purposes in either hyperactive or immunosuppressed populations. Here, we report a phenotypic screening of a human secretome library in human Treg cells utilising a high throughput flow cytometry technology. Screening a library of 575 secreted proteins allowed us to identify proteins stabilising or destabilising the Treg phenotype as suggested by changes in expression of Treg marker proteins FOXP3 and/or CTLA4. Four proteins including GDF-7, IL-10, PAP and IFNα-7 were identified as positive regulators that increased FOXP3 and/or CTLA4 expression. PAP is a phosphatase. A catalytic-dead version of the protein did not induce an increase in FOXP3 expression. Ten interferon proteins were identified as negative regulators that reduced the expression of both CTLA4 and FOXP3, without affecting cell viability. A transcriptomics analysis supported the differential effect on Tregs of IFNα-7 versus other IFNα proteins, indicating differences in JAK/STAT signaling. A conformational model experiment confirmed a tenfold reduction in IFNAR-mediated ISG transcription for IFNα-7 compared to IFNα-10. This further strengthened the theory of a shift in downstream messaging upon external stimulation. As a summary, we have identified four positive regulators of FOXP3 and/or CTLA4 expression. Further exploration of these Treg modulators and their method of action has the potential to aid the discovery of novel therapies for both autoimmune and infectious diseases as well as for cancer.

Identifiants

pubmed: 34408239
doi: 10.1038/s41598-021-96184-z
pii: 10.1038/s41598-021-96184-z
pmc: PMC8373891
doi:

Substances chimiques

Bone Morphogenetic Proteins 0
GDF7 protein, human 0
Growth Differentiation Factors 0
IFNA7 protein, human 0
Immunologic Factors 0
Interferon-alpha 0
Pancreatitis-Associated Proteins 0
REG3A protein, human 0

Types de publication

Journal Article Research Support, Non-U.S. Gov't

Langues

eng

Sous-ensembles de citation

IM

Pagination

16767

Informations de copyright

© 2021. The Author(s).

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Auteurs

Mei Ding (M)

Discovery Biology, Discovery Sciences, R&D, AstraZeneca, Gothenburg, Sweden. mei.ding@astrazeneca.com.

Rajneesh Malhotra (R)

Translational Science and Experimental Medicine, Research and Early Development, Respiratory and Immunology (R&I), BioPharmaceuticals R&D, AstraZeneca, Gothenburg, Sweden.

Tomas Ottosson (T)

Translational Science and Experimental Medicine, Research and Early Development, Respiratory and Immunology (R&I), BioPharmaceuticals R&D, AstraZeneca, Gothenburg, Sweden.

Magnus Lundqvist (M)

Department of Protein Science, School of Engineering Sciences in Chemistry, Biotechnology and Health, KTH - Royal Institute of Technology, Stockholm, Sweden.

Aman Mebrahtu (A)

Department of Protein Science, School of Engineering Sciences in Chemistry, Biotechnology and Health, KTH - Royal Institute of Technology, Stockholm, Sweden.

Johan Brengdahl (J)

Discovery Biology, Discovery Sciences, R&D, AstraZeneca, Gothenburg, Sweden.

Ulf Gehrmann (U)

Translational Science and Experimental Medicine, Research and Early Development, Respiratory and Immunology (R&I), BioPharmaceuticals R&D, AstraZeneca, Gothenburg, Sweden.

Elisabeth Bäck (E)

Mechanistic Biology and Profiling, Discovery Sciences, R&D, AstraZeneca, Gothenburg, Sweden.

Douglas Ross-Thriepland (D)

Discovery Biology, Discovery Sciences, R&D, AstraZeneca, Cambridge, UK.

Ida Isaksson (I)

Sample Management, Discovery Sciences, R&D, AstraZeneca, Gothenburg, Sweden.

Björn Magnusson (B)

Discovery Biology, Discovery Sciences, R&D, AstraZeneca, Gothenburg, Sweden.

Kris F Sachsenmeier (KF)

Translational Medicine, Oncology R&D, AstraZeneca, Boston, USA.

Hanna Tegel (H)

Department of Protein Science, School of Engineering Sciences in Chemistry, Biotechnology and Health, KTH - Royal Institute of Technology, Stockholm, Sweden.

Sophia Hober (S)

Department of Protein Science, School of Engineering Sciences in Chemistry, Biotechnology and Health, KTH - Royal Institute of Technology, Stockholm, Sweden.

Mathias Uhlén (M)

Department of Protein Science, School of Engineering Sciences in Chemistry, Biotechnology and Health, KTH - Royal Institute of Technology, Stockholm, Sweden.

Lorenz M Mayr (LM)

Discovery Biology, Discovery Sciences, R&D, AstraZeneca, Cambridge, UK.

Rick Davies (R)

Discovery Biology, Discovery Sciences, R&D, AstraZeneca, Cambridge, UK.

Johan Rockberg (J)

Department of Protein Science, School of Engineering Sciences in Chemistry, Biotechnology and Health, KTH - Royal Institute of Technology, Stockholm, Sweden.

Lovisa Holmberg Schiavone (LH)

Discovery Biology, Discovery Sciences, R&D, AstraZeneca, Gothenburg, Sweden. lovisa.holmberg.schiavone@astrazeneca.com.

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