Abstract
The loss of insulin-producing pancreatic β-cells in Type 1 diabetes mellitus (DM) is presumably the result of a T cell‒mediated process. In general, CD8+ T cells are the predominant lymphocytes in the insulitis lesions, and CD4+ T cell‒dominant insulitis is very rare. We present a case of a 72-year-old woman presented with excessive thirst and a 3-month history of weight loss. She was in a state of ketosis, and her plasma glucose concentration and HbA1c value were elevated. Moreover, anti-islet autoantibodies were positive, thus acute-onset Type 1 DM was diagnosed. At the time of diagnosis, a tumour was detected in the pancreas; total pancreatectomy was carried out 2 months later. The pathological diagnosis was intraductal papillary mucinous adenoma. Immunohistochemical staining of a sample of non-tumorous pancreatic tissue revealed 13 insulitis lesions infiltrated by both CD4+ and CD8+ T cells, and interestingly there were more CD4+ T cells than CD8+ T cells in the lesions. Moreover, B cells and macrophages had also infiltrated the lesions, and these two cell frequencies were both positively correlated with CD4+ as well as CD8+ T cell frequencies. This was a rare case with acute-onset Type 1 DM characterized by CD4+ T cell-dominant insulitis. Proinflammatory cytokines that can promote β-cell apoptosis or CD8+ T cell function are reported to be secreted from CD4+ T cells. Thus, together with B cells and macrophages, CD4+ T cell‒associated immune responses may have, directly and/or indirectly, played a role in the pathogenesis of the Type 1 DM in this patient.
| Original language | English |
|---|---|
| Pages (from-to) | 841-847 |
| Number of pages | 7 |
| Journal | Endocrine Journal |
| Volume | 63 |
| Issue number | 9 |
| DOIs | |
| Publication status | Published - 2016 |
Fingerprint
Keywords
- CD4 T cell
- Insulitis
- Pathogenesis
- Type 1 diabetes mellitus
ASJC Scopus subject areas
- Endocrinology, Diabetes and Metabolism
- Endocrinology
Cite this
CD4+ T cell‒dominant insulitis in acute-onset type 1 diabetes mellitus associated with intraductal papillary mucinous adenoma. / Yajima, Ken; Oikawa, Yoichi; Ogata, Kentaro; Hashiguchi, Akinori; Shimada, Akira.
In: Endocrine Journal, Vol. 63, No. 9, 2016, p. 841-847.Research output: Contribution to journal › Article
}
TY - JOUR
T1 - CD4+ T cell‒dominant insulitis in acute-onset type 1 diabetes mellitus associated with intraductal papillary mucinous adenoma
AU - Yajima, Ken
AU - Oikawa, Yoichi
AU - Ogata, Kentaro
AU - Hashiguchi, Akinori
AU - Shimada, Akira
PY - 2016
Y1 - 2016
N2 - The loss of insulin-producing pancreatic β-cells in Type 1 diabetes mellitus (DM) is presumably the result of a T cell‒mediated process. In general, CD8+ T cells are the predominant lymphocytes in the insulitis lesions, and CD4+ T cell‒dominant insulitis is very rare. We present a case of a 72-year-old woman presented with excessive thirst and a 3-month history of weight loss. She was in a state of ketosis, and her plasma glucose concentration and HbA1c value were elevated. Moreover, anti-islet autoantibodies were positive, thus acute-onset Type 1 DM was diagnosed. At the time of diagnosis, a tumour was detected in the pancreas; total pancreatectomy was carried out 2 months later. The pathological diagnosis was intraductal papillary mucinous adenoma. Immunohistochemical staining of a sample of non-tumorous pancreatic tissue revealed 13 insulitis lesions infiltrated by both CD4+ and CD8+ T cells, and interestingly there were more CD4+ T cells than CD8+ T cells in the lesions. Moreover, B cells and macrophages had also infiltrated the lesions, and these two cell frequencies were both positively correlated with CD4+ as well as CD8+ T cell frequencies. This was a rare case with acute-onset Type 1 DM characterized by CD4+ T cell-dominant insulitis. Proinflammatory cytokines that can promote β-cell apoptosis or CD8+ T cell function are reported to be secreted from CD4+ T cells. Thus, together with B cells and macrophages, CD4+ T cell‒associated immune responses may have, directly and/or indirectly, played a role in the pathogenesis of the Type 1 DM in this patient.
AB - The loss of insulin-producing pancreatic β-cells in Type 1 diabetes mellitus (DM) is presumably the result of a T cell‒mediated process. In general, CD8+ T cells are the predominant lymphocytes in the insulitis lesions, and CD4+ T cell‒dominant insulitis is very rare. We present a case of a 72-year-old woman presented with excessive thirst and a 3-month history of weight loss. She was in a state of ketosis, and her plasma glucose concentration and HbA1c value were elevated. Moreover, anti-islet autoantibodies were positive, thus acute-onset Type 1 DM was diagnosed. At the time of diagnosis, a tumour was detected in the pancreas; total pancreatectomy was carried out 2 months later. The pathological diagnosis was intraductal papillary mucinous adenoma. Immunohistochemical staining of a sample of non-tumorous pancreatic tissue revealed 13 insulitis lesions infiltrated by both CD4+ and CD8+ T cells, and interestingly there were more CD4+ T cells than CD8+ T cells in the lesions. Moreover, B cells and macrophages had also infiltrated the lesions, and these two cell frequencies were both positively correlated with CD4+ as well as CD8+ T cell frequencies. This was a rare case with acute-onset Type 1 DM characterized by CD4+ T cell-dominant insulitis. Proinflammatory cytokines that can promote β-cell apoptosis or CD8+ T cell function are reported to be secreted from CD4+ T cells. Thus, together with B cells and macrophages, CD4+ T cell‒associated immune responses may have, directly and/or indirectly, played a role in the pathogenesis of the Type 1 DM in this patient.
KW - CD4 T cell
KW - Insulitis
KW - Pathogenesis
KW - Type 1 diabetes mellitus
UR - http://www.scopus.com/inward/record.url?scp=84989172783&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=84989172783&partnerID=8YFLogxK
U2 - 10.1507/endocrj.EJ16-0192
DO - 10.1507/endocrj.EJ16-0192
M3 - Article
VL - 63
SP - 841
EP - 847
JO - Endocrine Journal
JF - Endocrine Journal
SN - 0918-8959
IS - 9
ER -