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Systemic autoimmunity and lymphoproliferation are associated with excess IL-7 and inhibited by IL-7R alpha blockade

Academic Article
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Overview

authors

  • Gonzalez-Quintial, R.
  • Lawson, Brian
  • Scatizzi, J. C.
  • Craft, J.
  • Kono, Dwight
  • Baccalà, Roberto
  • Theofilopoulos, Argyrios

publication date

  • November 2011

journal

  • PLoS One  Journal

abstract

  • Lupus is characterized by disturbances in lymphocyte homeostasis, as demonstrated by the marked accumulation of activated/memory T cells. Here, we provide evidence that proliferation of the CD8+ precursors for the accumulating CD4⁻CD8⁻ T cells in MRL-Fas(lpr) lupus-predisposed mice is, in part, driven by commensal antigens. The ensuing lymphadenopathy is associated with increased production of IL-7 due to expansion of fibroblastic reticular cells, the primary source of this cytokine. The excess IL-7 is not, however, consumed by CD4⁻CD8⁻ T cells due to permanent down-regulation of IL-7Rα (CD127), but instead supports proliferation of autoreactive T cells and progression of autoimmunity. Accordingly, IL-7R blockade reduced T cell activation and autoimmune manifestations even when applied at advanced disease stage. These findings indicate that an imbalance favoring production over consumption of IL-7 may contribute to systemic autoimmunity, and correction of this imbalance may be a novel therapeutic approach in lymphoproliferative and autoimmune syndromes.

subject areas

  • Animals
  • Autoimmunity
  • Blotting, Western
  • Enzyme-Linked Immunosorbent Assay
  • Flow Cytometry
  • Interleukin-7
  • Lymphatic Diseases
  • Lymphocyte Activation
  • Mice
  • Mice, Inbred C57BL
  • Mice, Inbred MRL lpr
  • RNA, Messenger
  • Real-Time Polymerase Chain Reaction
  • Receptors, Interleukin-7
  • T-Lymphocytes
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Identity

PubMed Central ID

  • PMC3213145

International Standard Serial Number (ISSN)

  • 1932-6203

Digital Object Identifier (DOI)

  • 10.1371/journal.pone.0027528

PubMed ID

  • 22102903
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Additional Document Info

start page

  • e27528

volume

  • 6

issue

  • 11

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