Identical TCR beta-chain rearrangements in streptococcal angina and skin lesions of patients with psoriasis vulgaris

J Immunol. 2006 Jun 1;176(11):7104-11. doi: 10.4049/jimmunol.176.11.7104.

Abstract

Tonsillar infection with Streptococcus pyogenes may induce several nonsuppurative autoimmune sequelae. The precise pathogenetic mechanisms behind this clinically well-established association are still unresolved. Using TCR analysis, we sought to identify a link between streptococcal tonsillitis and the T cell-mediated autoimmune response in psoriasis. Three patients with streptococcal-induced psoriasis underwent tonsillectomy. Using size spectratyping and sequencing of TCR beta-chain variable region gene (TCRBV) rearrangements, we compared the TCR usage of psoriatic skin lesions, blood, tonsils, and tonsillar T cells fractionated according to the expression of the skin address in "cutaneous lymphocyte-associated Ag" (CLA). TCRBV-size spectratype analysis of the blood lymphocytes, tonsils, and the CLA-negative tonsillar T cells revealed largely unselected T cell populations. Instead, TCRBV gene families of the psoriatic lesions and skin-homing CLA-positive tonsillar T cells displayed highly restricted spectratypes. Sequencing of TCRBV cDNA identified various clonal TCRBV rearrangements within the psoriatic lesions that indicated Ag-driven T cell expansion. Several of these clonotypes were also detected within the tonsils and, in one of the patients, within the small subset of CLA-positive tonsillar T cells, suggesting that T cells from the same T cell clones were simultaneously present within skin and tonsillar tissue. Because after tonsillectomy psoriasis cleared in all three patients our observations indicate that T cells may connect psoriatic inflammation to streptococcal angina. They suggest that the chronic streptococcal immune stimulus within the tonsils could act as a source for pathogenic T cells in poststreptococcal disorders, and they may help to explain why eliminating this source with tonsillectomy may improve streptococcal-induced sequelae.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Adult
  • Amino Acid Sequence
  • Antigens, Differentiation, T-Lymphocyte
  • Antigens, Neoplasm / genetics
  • Base Sequence
  • Clone Cells
  • Gene Rearrangement, beta-Chain T-Cell Antigen Receptor*
  • Humans
  • Membrane Glycoproteins / genetics
  • Molecular Sequence Data
  • Multigene Family
  • Palatine Tonsil / immunology
  • Palatine Tonsil / metabolism
  • Palatine Tonsil / pathology
  • Psoriasis / immunology*
  • Psoriasis / pathology*
  • Psoriasis / surgery
  • Receptors, Antigen, T-Cell, alpha-beta / biosynthesis*
  • Receptors, Antigen, T-Cell, alpha-beta / genetics
  • Receptors, Antigen, T-Cell, alpha-beta / isolation & purification*
  • Receptors, Lymphocyte Homing / genetics
  • Remission Induction
  • Rheumatic Heart Disease / immunology*
  • Rheumatic Heart Disease / pathology
  • Rheumatic Heart Disease / surgery
  • Severity of Illness Index
  • Streptococcal Infections / immunology*
  • Streptococcal Infections / pathology
  • Streptococcal Infections / surgery
  • Streptococcus pyogenes / immunology
  • T-Lymphocyte Subsets / immunology
  • T-Lymphocyte Subsets / metabolism*
  • T-Lymphocyte Subsets / pathology
  • Tonsillectomy
  • Tonsillitis / immunology
  • Tonsillitis / pathology
  • Tonsillitis / surgery

Substances

  • Antigens, Differentiation, T-Lymphocyte
  • Antigens, Neoplasm
  • CTAGE1 protein, human
  • Membrane Glycoproteins
  • Receptors, Antigen, T-Cell, alpha-beta
  • Receptors, Lymphocyte Homing