CXCL9/Mig mediates T cells recruitment to valvular tissue lesions of chronic rheumatic heart disease patients

Inflammation. 2013 Aug;36(4):800-11. doi: 10.1007/s10753-013-9606-2.

Abstract

Rheumatic fever (RF) is an autoimmune disease triggered by Streptococcus pyogenes infection frequently observed in infants from developing countries. Rheumatic heart disease (RHD), the major sequel of RF, leads to chronic inflammation of the myocardium and valvular tissue. T cells are the main population infiltrating cardiac lesions; however, the chemokines that orchestrate their recruitment are not clearly defined. Here, we investigated the expression of chemokines and chemokine receptors in cardiac tissue biopsies obtained from chronic RHD patients. Our results showed that CCL3/MIP1α gene expression was upregulated in myocardium while CCL1/I-309 and CXCL9/Mig were highly expressed in valvular tissue. Auto-reactive T cells that infiltrate valvular lesions presented a memory phenotype (CD4(+)CD45RO(+)) and migrate mainly toward CXCL9/Mig gradient. Collectively, our results show that a diverse milieu of chemokines is expressed in myocardium and valvular tissue lesions and emphasize the role of CXCL9/Mig in mediating T cell recruitment to the site of inflammation in the heart.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Adolescent
  • Adult
  • CD4-Positive T-Lymphocytes / immunology*
  • Cell Movement / immunology
  • Chemokine CCL1 / biosynthesis
  • Chemokine CCL1 / immunology
  • Chemokine CCL3 / biosynthesis
  • Chemokine CCL3 / immunology
  • Chemokine CXCL9 / biosynthesis
  • Chemokine CXCL9 / metabolism*
  • Child
  • Child, Preschool
  • Female
  • Fibrosis
  • Heart Valves / immunology*
  • Heart Valves / metabolism
  • Humans
  • Immunologic Memory / immunology
  • Male
  • Middle Aged
  • Myocardium / immunology*
  • Myocardium / metabolism
  • Neovascularization, Pathologic / immunology
  • Rheumatic Fever / immunology
  • Rheumatic Fever / microbiology
  • Rheumatic Heart Disease / immunology*
  • Streptococcus pyogenes
  • Young Adult

Substances

  • CCL1 protein, human
  • CCL3 protein, human
  • CXCL9 protein, human
  • Chemokine CCL1
  • Chemokine CCL3
  • Chemokine CXCL9