Diminished cytokine-induced Jak/STAT signaling is associated with rheumatoid arthritis and disease activity.

Rheumatoid arthritis (RA) is a systemic and incurable autoimmune disease characterized by chronic inflammation in synovial lining of joints. To identify the signaling pathways involved in RA, its disease activity, and treatment response, we adapted a systems immunology approach to simultaneously qua...

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Main Authors: Jason Ptacek, Rachael E Hawtin, Dongmei Sun, Brent Louie, Erik Evensen, Barbara B Mittleman, Alessandra Cesano, Guy Cavet, Clifton O Bingham, Stacey S Cofield, Jeffrey R Curtis, Maria I Danila, Chander Raman, Richard A Furie, Mark C Genovese, William H Robinson, Marc C Levesque, Larry W Moreland, Peter A Nigrovic, Nancy A Shadick, James R O'Dell, Geoffrey M Thiele, E William St Clair, Christopher C Striebich, Matthew B Hale, Houman Khalili, Franak Batliwalla, Cynthia Aranow, Meggan Mackay, Betty Diamond, Garry P Nolan, Peter K Gregersen, S Louis Bridges
Format: Article
Language:English
Published: Public Library of Science (PLoS) 2021-01-01
Series:PLoS ONE
Online Access:https://journals.plos.org/plosone/article/file?id=10.1371/journal.pone.0244187&type=printable
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author Jason Ptacek
Rachael E Hawtin
Dongmei Sun
Brent Louie
Erik Evensen
Barbara B Mittleman
Alessandra Cesano
Guy Cavet
Clifton O Bingham
Stacey S Cofield
Jeffrey R Curtis
Maria I Danila
Chander Raman
Richard A Furie
Mark C Genovese
William H Robinson
Marc C Levesque
Larry W Moreland
Peter A Nigrovic
Nancy A Shadick
James R O'Dell
Geoffrey M Thiele
E William St Clair
Christopher C Striebich
Matthew B Hale
Houman Khalili
Franak Batliwalla
Cynthia Aranow
Meggan Mackay
Betty Diamond
Garry P Nolan
Peter K Gregersen
S Louis Bridges
author_facet Jason Ptacek
Rachael E Hawtin
Dongmei Sun
Brent Louie
Erik Evensen
Barbara B Mittleman
Alessandra Cesano
Guy Cavet
Clifton O Bingham
Stacey S Cofield
Jeffrey R Curtis
Maria I Danila
Chander Raman
Richard A Furie
Mark C Genovese
William H Robinson
Marc C Levesque
Larry W Moreland
Peter A Nigrovic
Nancy A Shadick
James R O'Dell
Geoffrey M Thiele
E William St Clair
Christopher C Striebich
Matthew B Hale
Houman Khalili
Franak Batliwalla
Cynthia Aranow
Meggan Mackay
Betty Diamond
Garry P Nolan
Peter K Gregersen
S Louis Bridges
author_sort Jason Ptacek
collection DOAJ
description Rheumatoid arthritis (RA) is a systemic and incurable autoimmune disease characterized by chronic inflammation in synovial lining of joints. To identify the signaling pathways involved in RA, its disease activity, and treatment response, we adapted a systems immunology approach to simultaneously quantify 42 signaling nodes in 21 immune cell subsets (e.g., IFNα→p-STAT5 in B cells) in peripheral blood mononuclear cells (PBMC) from 194 patients with longstanding RA (including 98 patients before and after treatment), and 41 healthy controls (HC). We found multiple differences between patients with RA compared to HC, predominantly in cytokine-induced Jak/STAT signaling in many immune cell subsets, suggesting pathways that may be associated with susceptibility to RA. We also found that high RA disease activity, compared to low disease activity, was associated with decreased (e.g., IFNα→p-STAT5, IL-10→p-STAT1) or increased (e.g., IL-6→STAT3) response to stimuli in multiple cell subsets. Finally, we compared signaling in patients with established, refractory RA before and six months after initiation of methotrexate (MTX) or TNF inhibitors (TNFi). We noted significant changes from pre-treatment to post-treatment in IFNα→p-STAT5 signaling and IL-10→p-STAT1 signaling in multiple cell subsets; these changes brought the aberrant RA signaling profiles toward those of HC. This large, comprehensive functional signaling pathway study provides novel insights into the pathogenesis of RA and shows the potential of quantification of cytokine-induced signaling as a biomarker of disease activity or treatment response.
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spelling doaj-art-9b1ea73e854343108c3cc3ca29f2e25a2025-08-20T02:55:13ZengPublic Library of Science (PLoS)PLoS ONE1932-62032021-01-01161e024418710.1371/journal.pone.0244187Diminished cytokine-induced Jak/STAT signaling is associated with rheumatoid arthritis and disease activity.Jason PtacekRachael E HawtinDongmei SunBrent LouieErik EvensenBarbara B MittlemanAlessandra CesanoGuy CavetClifton O BinghamStacey S CofieldJeffrey R CurtisMaria I DanilaChander RamanRichard A FurieMark C GenoveseWilliam H RobinsonMarc C LevesqueLarry W MorelandPeter A NigrovicNancy A ShadickJames R O'DellGeoffrey M ThieleE William St ClairChristopher C StriebichMatthew B HaleHouman KhaliliFranak BatliwallaCynthia AranowMeggan MackayBetty DiamondGarry P NolanPeter K GregersenS Louis BridgesRheumatoid arthritis (RA) is a systemic and incurable autoimmune disease characterized by chronic inflammation in synovial lining of joints. To identify the signaling pathways involved in RA, its disease activity, and treatment response, we adapted a systems immunology approach to simultaneously quantify 42 signaling nodes in 21 immune cell subsets (e.g., IFNα→p-STAT5 in B cells) in peripheral blood mononuclear cells (PBMC) from 194 patients with longstanding RA (including 98 patients before and after treatment), and 41 healthy controls (HC). We found multiple differences between patients with RA compared to HC, predominantly in cytokine-induced Jak/STAT signaling in many immune cell subsets, suggesting pathways that may be associated with susceptibility to RA. We also found that high RA disease activity, compared to low disease activity, was associated with decreased (e.g., IFNα→p-STAT5, IL-10→p-STAT1) or increased (e.g., IL-6→STAT3) response to stimuli in multiple cell subsets. Finally, we compared signaling in patients with established, refractory RA before and six months after initiation of methotrexate (MTX) or TNF inhibitors (TNFi). We noted significant changes from pre-treatment to post-treatment in IFNα→p-STAT5 signaling and IL-10→p-STAT1 signaling in multiple cell subsets; these changes brought the aberrant RA signaling profiles toward those of HC. This large, comprehensive functional signaling pathway study provides novel insights into the pathogenesis of RA and shows the potential of quantification of cytokine-induced signaling as a biomarker of disease activity or treatment response.https://journals.plos.org/plosone/article/file?id=10.1371/journal.pone.0244187&type=printable
spellingShingle Jason Ptacek
Rachael E Hawtin
Dongmei Sun
Brent Louie
Erik Evensen
Barbara B Mittleman
Alessandra Cesano
Guy Cavet
Clifton O Bingham
Stacey S Cofield
Jeffrey R Curtis
Maria I Danila
Chander Raman
Richard A Furie
Mark C Genovese
William H Robinson
Marc C Levesque
Larry W Moreland
Peter A Nigrovic
Nancy A Shadick
James R O'Dell
Geoffrey M Thiele
E William St Clair
Christopher C Striebich
Matthew B Hale
Houman Khalili
Franak Batliwalla
Cynthia Aranow
Meggan Mackay
Betty Diamond
Garry P Nolan
Peter K Gregersen
S Louis Bridges
Diminished cytokine-induced Jak/STAT signaling is associated with rheumatoid arthritis and disease activity.
PLoS ONE
title Diminished cytokine-induced Jak/STAT signaling is associated with rheumatoid arthritis and disease activity.
title_full Diminished cytokine-induced Jak/STAT signaling is associated with rheumatoid arthritis and disease activity.
title_fullStr Diminished cytokine-induced Jak/STAT signaling is associated with rheumatoid arthritis and disease activity.
title_full_unstemmed Diminished cytokine-induced Jak/STAT signaling is associated with rheumatoid arthritis and disease activity.
title_short Diminished cytokine-induced Jak/STAT signaling is associated with rheumatoid arthritis and disease activity.
title_sort diminished cytokine induced jak stat signaling is associated with rheumatoid arthritis and disease activity
url https://journals.plos.org/plosone/article/file?id=10.1371/journal.pone.0244187&type=printable
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