Macrophages and dendritic cells infiltrating islets with or without beta cells produce tumour necrosis factor-α in patients with recent-onset type 1 diabetes
2007
Uno, S | Imagawa, A | Okita, K | Sayama, K | Moriwaki, M | Iwahashi, H | Yamagata, K | Tamura, S | Matsuzawa, Y | Hanafusa, T | Miyagawa, J | Shimomura, I
Aims/hypothesis 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. Materials and methods We obtained pancreatic biopsy specimens from six patients with recent-onset type 1 diabetes and analysed these by immunohistochemistry. Results 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]). Conclusions/interpretation Macrophages and dendritic cells infiltrate the islets and produce inflammatory cytokines (TNF-α and IL-1β) during the development of type 1A diabetes.
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