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Research article
Gang Tian
Xi'an Jiaotong University Medical College First Affiliated Hospital
Corresponding Author
ORCiD: https://orcid.org/0000-0003-4841-4694
License:
This work is licensed under a CC BY 4.0 License. Read Full License
Background
Interleukin-35 (IL-35) is a newly identified IL-12 cytokine family member, which regulates the activity of immune cells in infectious diseases and autoimmune disorders. However, the regulatory function of IL-35 in Kawasaki disease is not well elucidated.
Methods
Thirty-three patients with Kawasaki disease and seventeen healthy controls were studied. Peripheral IL-35 concentration was measured by enzyme linked immunosorbent assay. CD14 + monocytes were purified, and mRNA expression of IL-35 receptor (IL-12Rβ2 and gp130) was semi-quantified by real-time polymerase chain reaction. CD14 + monocytes were stimulated with recombinant IL-35. The modulatory role of IL-35 treated CD14 + monocytes to naïve CD4 + T cell activation was investigated by flow cytometry. The influence of IL-35 to cytotoxicity of CD14 + monocytes was assessed by measuring target cell death, cytokine and granzyme secretion.
Results
Plasma IL-35 concentration was elevated in patients with Kawasaki disease. There was no significant differences of either IL-12Rβ2 or gp130 mRNA expression in CD14 + monocytes between Kawasaki disease patients and controls. IL-35 suppressed CD14 + monocytes induced naïve CD4 + T cell activation in Kawasaki disease, and this process required direct cell-to-cell contact. IL-35 also inhibited tumor necrosis factor-α (TNF-α) and granzyme B secretion by CD14 + monocytes from patients with Kawasaki disease, however, only granzyme B was responsible for the cytotoxicity of CD14 + monocytes.
Conclusions
IL-35 played an important immunosuppressive role to CD14 + monocytes function in Kawasaki disease.
Keywords
Kawasaki disease; interleukin-35; monocytes; immunosuppression
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CURRENT STATUS: Published
View the published article at BMC Immunology.
Version 2
Posted 24 Feb, 2020
No community comments so far
Review #1 received
Received 09 Mar, 2020
Reviewer #1 agreed
On 27 Feb, 2020
Editor assigned
On 24 Feb, 2020
Reviewers invited
Invitations sent on 24 Feb, 2020
Submission checks complete
On 23 Feb, 2020
Editor invited
On 23 Feb, 2020
No comments provided
Editorial decision: Major revision
On 19 Feb, 2020
Review #2 received
Received 17 Feb, 2020
Review #1 received
Received 10 Feb, 2020
Reviewer #2 agreed
On 06 Feb, 2020
Reviewer #1 agreed
On 31 Jan, 2020
Reviewers invited
Invitations sent on 13 Jan, 2020
Submission checks complete
On 17 Dec, 2019
Editor invited
On 16 Dec, 2019
Editor assigned
On 12 Dec, 2019
First submitted
On 11 Dec, 2019
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A new preprint design is coming!
We have improved readability, clarity, accessibility, and opportunities for engagement.
See the published version of this preprint at BMC Immunology.
This is a preprint, a preliminary version of a manuscript that has not completed peer review at a journal. Research Square does not conduct peer review prior to posting preprints. The posting of a preprint on this server should not be interpreted as an endorsement of its validity or suitability for dissemination as established information or for guiding clinical practice.
Learn more about In Review
Research article
Gang Tian
Xi'an Jiaotong University Medical College First Affiliated Hospital
Corresponding Author
ORCiD: https://orcid.org/0000-0003-4841-4694
Badges
Prescreen
This manuscript passed our Prescreen assessment
Complete author information
Appropriate declaration statements
Potential risks to human health
Prescreen
Peer Review Timeline
CURRENT STATUS: Published
View the published article at BMC Immunology.
Version 2
Posted 24 Feb, 2020
No community comments so far
Review #1 received
Received 09 Mar, 2020
Reviewer #1 agreed
On 27 Feb, 2020
Editor assigned
On 24 Feb, 2020
Reviewers invited
Invitations sent on 24 Feb, 2020
Submission checks complete
On 23 Feb, 2020
Editor invited
On 23 Feb, 2020
No comments provided
Editorial decision: Major revision
On 19 Feb, 2020
Review #2 received
Received 17 Feb, 2020
Review #1 received
Received 10 Feb, 2020
Reviewer #2 agreed
On 06 Feb, 2020
Reviewer #1 agreed
On 31 Jan, 2020
Reviewers invited
Invitations sent on 13 Jan, 2020
Submission checks complete
On 17 Dec, 2019
Editor invited
On 16 Dec, 2019
Editor assigned
On 12 Dec, 2019
First submitted
On 11 Dec, 2019
Metrics
Comments: 0
PDF Downloads: ...
HTML Views: ...
License:
This work is licensed under a CC BY 4.0 License. Read Full License
View the published article at BMC Immunology.
Background
Interleukin-35 (IL-35) is a newly identified IL-12 cytokine family member, which regulates the activity of immune cells in infectious diseases and autoimmune disorders. However, the regulatory function of IL-35 in Kawasaki disease is not well elucidated.
Methods
Thirty-three patients with Kawasaki disease and seventeen healthy controls were studied. Peripheral IL-35 concentration was measured by enzyme linked immunosorbent assay. CD14 + monocytes were purified, and mRNA expression of IL-35 receptor (IL-12Rβ2 and gp130) was semi-quantified by real-time polymerase chain reaction. CD14 + monocytes were stimulated with recombinant IL-35. The modulatory role of IL-35 treated CD14 + monocytes to naïve CD4 + T cell activation was investigated by flow cytometry. The influence of IL-35 to cytotoxicity of CD14 + monocytes was assessed by measuring target cell death, cytokine and granzyme secretion.
Results
Plasma IL-35 concentration was elevated in patients with Kawasaki disease. There was no significant differences of either IL-12Rβ2 or gp130 mRNA expression in CD14 + monocytes between Kawasaki disease patients and controls. IL-35 suppressed CD14 + monocytes induced naïve CD4 + T cell activation in Kawasaki disease, and this process required direct cell-to-cell contact. IL-35 also inhibited tumor necrosis factor-α (TNF-α) and granzyme B secretion by CD14 + monocytes from patients with Kawasaki disease, however, only granzyme B was responsible for the cytotoxicity of CD14 + monocytes.
Conclusions
IL-35 played an important immunosuppressive role to CD14 + monocytes function in Kawasaki disease.
Figure 1
Figure 2
Figure 3
Figure 4
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