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Altered peptide ligands regulate muscarinic acetylcholine receptor reactive T cells of patients with Sjögren’s syndrome
  1. Y Naito,
  2. I Matsumoto,
  3. E Wakamatsu,
  4. D Goto,
  5. S Ito,
  6. A Tsutsumi,
  7. T Sumida
  1. Department of Internal Medicine, University of Tsukuba, Tsukuba, Japan
  1. Correspondence to:
    Professor T Sumida
    Department of Internal Medicine, University of Tsukuba, 1-1-1 Tennodai, Tsukuba City, Ibaraki 305-8575, Japan; tsumida{at}md.tsukuba.ac.jp

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In the generation of Sjögren’s syndrome (SS), CD4 positive αβ T cells have a crucial role. Previous studies have provided evidence about the T cell receptor (TCR) Vβ and Vα genes on these T cells, and sequence analysis of the CDR3 region indicates the presence of some conserved amino acid motifs, supporting the notion that infiltrating T cells recognise relatively few epitopes on autoantigens.1

Candidate autoantigens recognised by T cells that infiltrate the labial salivary glands of patients with SS have been analysed, and Ro/SSA 52 kDa,2 α-amylase, heat shock protein, and TCR BV6 have been identified, although Ro/SSA 52 kDa reactive T cells were not increased in peripheral blood.3 Gordon et al indicated that anti-M3R autoantibodies occurred in SS and were associated with the sicca symptoms.4 Recently, we provided evidence for the presence of autoantibodies against the second extracellular domain of muscarinic acetylcholine receptor (M3R) in a subgroup of patients with SS.5 The M3R is an interesting molecule, because this portion has an important role in intracellular signalling,5 although the function of anti-M3R autoantibodies remains unknown.

The mechanism through which a peptide is recognised by a TCR is flexible. If the amino acid residue of the peptide ligands for TCR is substituted by a different amino acid and can still …

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