Journal of the Pancreas Open Access

  • ISSN: 1590-8577
  • Journal h-index: 82
  • Journal CiteScore: 35.06
  • Journal Impact Factor: 24.75
  • Average acceptance to publication time (5-7 days)
  • Average article processing time (30-45 days) Less than 5 volumes 30 days
    8 - 9 volumes 40 days
    10 and more volumes 45 days

Abstract

Possible Involvement of Innate Lymphoid Cells in the Development of Chronic Inflammatory Pancreatic Diseases

Manami Ikemune, Kazushige Uchida, Masato Yanagawa, Satoshi Tsukuda, Takashi Tomiyama, Toshihiro Tanaka, Yugo Ando, Tsukasa Ikeura, Takashi Yamaguchi, Toshiro Fukui, Akiyoshi Nishio, Kazuichi Okazaki

Introduction Type 1 autoimmune pancreatitis is a chronic fibro-inflammatory disorder. We previously reported the involvement of M2 macrophages and basophils in autoimmune pancreatitis. It is reported that Group 2 innate lymphoid cells (ILC2s) and basophils play an important role in asthma. Thus, this study investigated the roles of innate lymphoid cells in autoimmune pancreatitis. Subjects and methods We recruited 28 patients with autoimmune pancreatitis (25 men and 3 women; mean age, 68.4 years) who were not receiving steroid therapy, 10 patients with chronic pancreatitis (CP; 2 women and 3 men with idiopathic CP and 5 men with alcoholic CP; mean age, 65.9 years), and 30 healthy controls (HCs; 5 women and 25 men; mean age, 66.9 years). Peripheral ILCs were analyzed using flow cytometry. We also analyzed two types of ILC2s (lineage− CD127+ CD161+ c-Kit+/− CRTH2+ and lineage− CD25+ IL-33R+ cells). Results The proportions of ILC2s and ILC3s were significantly higher in the autoimmune pancreatitis (0.140% ± 0.083% and 0.055% ± 0.043%, respectively) and CP groups (0.119% ± 0.055% and 0.051% ± 0.040%, respectively) than in the HC group (0.054% ± 0.039% and 0.018% ± 0.017%, respectively). The proportion of ILC1s did not differ among three groups. There was no significant correlation between the counts of the two ILC2 types. Conclusion Elevated ILC2 and ILC3 counts may be involved in the development of chronic pancreatic inflammation.