Increased CCL25 and T Helper Cells Expressing CCR9 in the Salivary Glands of Patients With Primary Sjögren's Syndrome: Potential New Axis in Lymphoid Neogenesis

Arthritis Rheumatol. 2017 Oct;69(10):2038-2051. doi: 10.1002/art.40182. Epub 2017 Aug 29.

Abstract

Objective: Follicular helper T (Tfh) cells play a critical role in germinal center formation and B cell activation, both of which are hallmarks of primary Sjögren's syndrome (SS). CCR9-expressing T helper cells have "Tfh-like" characteristics and their numbers are increased at mucosa-associated sites in several inflammatory conditions. Because the characteristics of these cells are unique and evaluation has been limited, this study was undertaken to investigate the local and systemic CCL25/CCR9 axis in patients with primary SS.

Methods: Levels of CCL25 protein and messenger RNA (mRNA) and CCR9+ T helper cells were evaluated in the labial salivary glands (LSGs) of patients with primary SS and patients with sicca syndrome without a diagnosis of primary SS (non-SS sicca controls). CCL25 levels were assessed for correlation with parameters of inflammation and clinical features. Circulating CCR9+ and CXCR5+ T helper cells were compared on the basis of phenotypic and functional properties.

Results: CCL25 protein and mRNA levels were elevated in the LSGs of patients with primary SS as compared to non-SS sicca controls. Increased levels of CCL25 were associated with B cell hyperactivity, autoimmunity, and levels of interleukin-21 (IL-21) and soluble IL-7 receptor α-chain (IL-7Rα). Furthermore, the frequency of CCR9-expressing cells in the LSGs was increased and levels of circulating CCR9+ T helper cells expressing programmed death 1 and inducible T cell costimulator were elevated in patients with primary SS. CCR9+ T helper cells displayed higher expression of IL-7Rα and secreted higher levels of interferon-γ, IL-17, IL-4, and IL-21 as compared to CXCR5+ T helper cells, ex vivo and upon triggering with antigen or IL-7. Both CCR9+ and CXCR5+ T helper cells induced IgG production by B cells more potently than that induced in the cultures with CCR9-CXCR5- T helper cells.

Conclusion: Enhanced expression of CCL25 in LSGs of patients with primary SS can facilitate attraction of CCR9+ T helper cells, and these cells secrete high levels of proinflammatory cytokines when triggered with antigen or IL-7. The observed associations with B cell hyperactivity, autoimmunity, and markers of lymphoid neogenesis indicate that the CCL25/CCR9 axis plays a significant role in the immunopathology of primary SS, suggesting that this axis could represent a novel therapeutic target for the disease.

MeSH terms

  • Adult
  • Aged
  • Autoimmunity / immunology
  • B-Lymphocytes / immunology
  • Case-Control Studies
  • Chemokines, CC / genetics
  • Chemokines, CC / immunology*
  • Female
  • Humans
  • Immunoglobulin G / immunology
  • Inducible T-Cell Co-Stimulator Protein / immunology
  • Interferon-gamma / immunology
  • Interleukin-17 / immunology
  • Interleukin-4 / immunology
  • Interleukin-7 Receptor alpha Subunit / immunology
  • Interleukins / immunology
  • Lip
  • Male
  • Middle Aged
  • Programmed Cell Death 1 Receptor / immunology
  • RNA, Messenger
  • Receptors, CCR / immunology
  • Receptors, CXCR5 / immunology
  • Salivary Glands, Minor / immunology*
  • Sjogren's Syndrome / immunology*
  • T-Lymphocytes, Helper-Inducer / immunology*

Substances

  • CC chemokine receptor 9
  • CCL25 protein, human
  • CXCR5 protein, human
  • Chemokines, CC
  • IL4 protein, human
  • Immunoglobulin G
  • Inducible T-Cell Co-Stimulator Protein
  • Interleukin-17
  • Interleukin-7 Receptor alpha Subunit
  • Interleukins
  • PDCD1 protein, human
  • Programmed Cell Death 1 Receptor
  • RNA, Messenger
  • Receptors, CCR
  • Receptors, CXCR5
  • Interleukin-4
  • Interferon-gamma
  • interleukin-21