Macrophages and dendritic cells infiltrating islets with or without beta cells produce tumour necrosis factor-α in patients with recent-onset type 1 diabetes

Springer Science and Business Media LLC - Tập 50 - Trang 596-601 - 2007
S. Uno1, A. Imagawa1,2, K. Okita1, K. Sayama1, M. Moriwaki3, H. Iwahashi1, K. Yamagata1, S. Tamura4, Y. Matsuzawa5, T. Hanafusa2, J. Miyagawa6, I. Shimomura1
1Department of Metabolic Medicine, Graduate School of Medicine, Osaka University, Suita, Japan
2First Department of Internal Medicine, Osaka Medical College, Takatsuki, Japan
3Department of Internal Medicine, Mino City Hospital, Mino, Japan
4Department of Gastroenterology and Hepatology, Graduate School of Medicine, Osaka University, Suita, Japan
5Sumitomo Hospital, Osaka, Japan
6Division of Diabetes and Metabolism, Internal Medicine, Hyogo College of Medicine, Nishinomiya, Japan

Tóm tắt

Type 1A diabetes results from autoimmune destruction of pancreatic beta cells. We examined the involvement of TNF-α and IL-1β, as well as of T cells, macrophages and dendritic cells, in the destruction of beta cells in patients with recent-onset type 1 diabetes. We obtained pancreatic biopsy specimens from six patients with recent-onset type 1 diabetes and analysed these by immunohistochemistry. T cell infiltration was less common in islets without beta cells (12.5 [0–33.3]%) than in those with beta cells (46.0 [17.4–83.3]%), while macrophages and dendritic cells showed a similar extent of infiltration into islets both with or without beta cells. TNF-α was detected in 25.0 (4.3–46.9)% of macrophages and 11.8 (0–40.0)% of dendritic cells infiltrating the islets in samples from each patient, but not at all in T cells. IL-1β was detected in 1.8 (0–11.3)% of T cells infiltrating the islets with beta cells, while it was found in 19.2 (0–35.3)% of macrophages or 10.7 (0–31.3)% of dendritic cells infiltrating the islets in samples from each patient (all values median [range]). Macrophages and dendritic cells infiltrate the islets and produce inflammatory cytokines (TNF-α and IL-1β) during the development of type 1A diabetes.

Tài liệu tham khảo

Eisenbarth GS (1986) Type I diabetes mellitus. A chronic autoimmune disease. N Engl J Med 314:1360–1368 Hanafusa T, Miyazaki A, Miyagawa J et al (1990) Examination of islets in the pancreas biopsy specimens from newly diagnosed type 1 (insulin-dependent) diabetic patients. Diabetologia 33:105–111 Thomas HE, Darwiche R, Corbett JA, Kay TW (1999) Evidence that beta cell death in nonobese diabetic mouse is Fas independent. J Immunol 163:1562–1569 Jiang Z, Woda BA (1991) Cytokine gene expression in the islets of the diabetic Biobreeding/Worcester rat. J Immunol 146:2990–2994 Iwahashi H, Hanafusa T, Eguchi Y et al (1996) Cytokine-induced apoptotic cell death in a mouse pancreatic beta-cell line: inhibition by Bcl-2. Diabetologia 39:530–536 Corbett JA, Wang JL, Sweetland MA, Lancaster JR Jr, McDaniel ML (1992) Interleukin-1 beta induces the formation of nitric oxide by beta-cells purified from rodent islets of Langerhans. Evidence for the beta-cell as a source and site of action of nitric oxide. J Clin Invest 90:2384–2391 Yang XD, Tisch R, Singer SM et al (1994) Effect of tumor necrosis factor alpha on insulin-dependent diabetes mellitus in NOD mice. 1. The early development of autoimmunity and the diabetogenic process. J Exp Med 180:995–1004 Kagi D, Ho A, Odermatt B, Zakarian A, Ohashi PS, Mak TW (1999) TNF receptor 1-dependent beta cell toxicity as an effector pathway in autoimmune diabetes. J Immunol 162:4598–4605 Cailleau C, Diu-Hercend A, Ruuth E, Westwood R, Carnaud C (1997) Treatment with neutralizing antibodies specific for IL-1beta prevents cyclophosphamide-induced diabetes in nonobese diabetic mice. Diabetes 46:937–940 Thomas HE, Irawaty W, Darwiche R et al (2004) IL-1 receptor deficiency slows progression to diabetes in the NOD mouse. Diabetes 53:113–121 Sandberg JO, Eizirik DL, Sandler S (1997) IL-1 receptor antagonist inhibits recurrence of disease after syngeneic pancreatic islet transplantation to spontaneously diabetic non-obese diabetic (NOD) mice. Clin Exp Immunol 108:314–317 Yamagata K, Nakajima H, Tomita K et al (1996) Dominant TCR alpha-chain clonotypes and interferon-gamma are expressed in the pancreas of patients with recent-onset insulin-dependent diabetes mellitus. Diabetes Res Clin Pract 34:37–46 Alberti KG, Zimmet PZ (1998) Definition, diagnosis and classification of diabetes mellitus and its complications. Part 1: diagnosis and classification of diabetes mellitus. Provisional report of a WHO consultation. Diabet Med 15:539–553 Imagawa A, Hanafusa T, Tamura S et al (2001) Pancreatic biopsy as a procedure for detecting in situ autoimmune phenomena in type 1 diabetes: close correlation between serological markers and histological evidence of cellular autoimmunity. Diabetes 50:1269–1273 Itoh N, Hanafusa T, Miyazaki A et al (1993) Mononuclear cell infiltration and its relation to the expression of major histocompatibility complex antigens and adhesion molecules in pancreas biopsy specimens from newly diagnosed insulin-dependent diabetes mellitus patients. J Clin Invest 92:2313–2322 Stassi G, Todaro M, Richiusa P et al (1995) Expression of apoptosis-inducing CD95 (Fas/Apo-1) on human beta-cells sorted by flow-cytometry and cultured in vitro. Transplant Proc 27:3271–3275 Moriwaki M, Itoh N, Miyagawa J et al (1999) Fas and Fas ligand expression in inflamed islets in pancreas sections of patients with recent-onset type 1 diabetes mellitus. Diabetologia 42:1332–1340 Calafiore R, Pietropaolo M, Basta G, Falorni A, Picchio ML, Brunetti P (1993) Pancreatic beta-cell destruction in non-obese diabetic mice. Metabolism 42:854–859 Nakayama M, Abiru N, Moriyama H et al (2005) Prime role for an insulin epitope in the development of type 1 diabetes in NOD mice. Nature 435:151–152 Banchereau J, Steinman RM (1998) Dendritic cells and the control of immunity. Nature 392:245–252 Dahlen E, Dawe K, Ohlsson L, Hedlund G (1998) Dendritic cells and macrophages are the first and major producers of TNF-alpha in pancreatic islets in the nonobese diabetic mouse. J Immunol 160:3585–3593