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Production of IL‐16 Correlates with CD3+ T Cell Infiltration in Pancreatic Islets of Diabetic Rats
Author(s) -
Skundric Dusanka,
Dai Rujuan,
Zhou Weili
Publication year - 2008
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.22.2_supplement.453
Subject(s) - pancreatic islets , medicine , immune system , immunology , islet , type 1 diabetes , cd8 , endocrinology , cytokine , diabetes mellitus
Type I diabetes mellitus (T1DM) is a CD4+ Th1 mediated autoimmune disease. Homing of inflammatory cells to pancreatic islets is orchestrated by locally produced chemoattractant cues. A cytokine, IL‐16 is elaborated by activated T cells and it specifically regulates homing of CD4+ T cells. We reported an important role of IL‐16 in immune regulation of CD4+ Th1 mediated autoimmune disease, multiple sclerosis. Role of IL‐16 in immunopathogenesis of T1DM remains unknown. In this study we investigated presence and cellular sources of IL‐16 in pancreatic islets of Bio Breeding ‐ Diabetes Prone (BBDP), and compared to congenic diabetes resistant (BBDR) rats. By two‐color immunostaining and con‐focal analysis, we observed IL‐16 immunoreactivity exclusively in islets of diabetic BBDP but not BBDR, or prediabetic BBDP rats. IL‐16 co‐localized well with infiltrating CD4+ and CD8+ T cells, thus suggesting that IL‐16 was mostly elaborated by infiltrating CD3+ T cells. Conversely, IL‐16 did not co‐localize with insulin containing β‐cells. An increase in IL‐16 immunoreactivity correlated with reduction of β‐cells mass. Our data suggest production of IL‐16, by infiltrating CD3+ T cells, and reveal potentially important role of IL‐16 in immunopathogenesis of T1DM This study was supported by the Parker Webber endowment for the Department of Neurology and DMC, and by funds from the Department of Internal medicine – Endocrinology WSU.