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Targeting the RhoA-ROCK pathway to reverse T-cell dysfunction in SLE.

Cristina Rozo1, Yurii Chinenov2,3, Reena Khianey Maharaj1

  • 1Autoimmunity and Inflammation Program, Hospital for Special Surgery, New York, New York, USA.

Annals of the Rheumatic Diseases
|March 12, 2017
PubMed
Summary

Elevated Rho-associated kinase (ROCK) activity is found in systemic lupus erythematosus (SLE) and rheumatoid arthritis (RA). Targeting the ROCK pathway effectively reduces the production of key inflammatory cytokines IL-17 and IL-21.

Keywords:
AutoimmunitySystemic Lupus ErythematosusT Cells

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Area of Science:

  • Immunology
  • Molecular Biology
  • Rheumatology

Background:

  • Interleukin (IL)-17 and IL-21 dysregulation is implicated in autoimmune diseases like systemic lupus erythematosus (SLE) and rheumatoid arthritis (RA).
  • Rho-associated kinase 2 (ROCK2) is a key regulator of IL-17 and IL-21 production.
  • Previous studies indicated increased ROCK activation in SLE patients.

Purpose of the Study:

  • To evaluate Rho-associated kinase (ROCK) activity in new cohorts of SLE and rheumatoid arthritis (RA) patients.
  • To assess the efficacy of different ROCK pathway inhibitors in suppressing IL-17 and IL-21 production by T cells from SLE patients and human Th17 cells.

Main Methods:

  • ROCK activity was measured in peripheral blood mononuclear cells (PBMCs) from SLE, RA patients, and healthy controls using ELISA.
  • SLE T cells and in vitro-differentiated Th17 cells were treated with ROCK inhibitors (Y27632, KD025, simvastatin).
  • IL-17 and IL-21 production, ROCK activity, and transcriptional profiles were analyzed.

Main Results:

  • Significantly higher ROCK activity was observed in PBMCs from SLE and RA patients compared to healthy controls.
  • All tested ROCK inhibitors (Y27632, KD025, simvastatin) reduced ROCK activity and suppressed IL-17 and IL-21 production in Th17 cells and SLE T cells.
  • Distinct and overlapping effects of ROCK inhibitors on immune cell transcriptional profiles were identified.

Conclusions:

  • Elevated ROCK activity is a characteristic feature in patients with SLE and RA.
  • Targeting the RhoA-ROCK pathway, using either non-selective or selective inhibitors, can effectively reduce IL-17 and IL-21 production in SLE T cells and Th17 cells.