Abstract
To investigate host leukocytes recruited to the pancreas by diabetogenic T cells, we administered islet-specific CD4+ T cell clones to 2-week-old nonobese diabetic (NOD) mice and examined the resulting pancreatic infiltrate by flow cytometry. Two different Vβ4+CD4+ T cell clones, BDC 2.5 and BDC 6.9, were found to recruit a heterogeneous T cell population as determined by staining with a panel of anti-TCR Vβ monoclonal antibodies. The majority of the diabetes-initiating, Vβ4+ T cell clones migrated to the spleen whereas only 5-8% of the T cell population infiltrating the pancreas was Vβ4+. Anti-IL-2 receptor staining indicated that fewer than 10% of the total population of infiltrating lymphocytes within the pancreas were in a highly activated state. We have further found that normal splenic T cells from the NOD mouse proliferate poorly to IL-2 in vitro, yet secrete IFN-γ in response to IL-2 stimulation. These results suggest that the recruited host T cells in our disease transfer system are not directly pathogenic but, rather, are responding to the small numbers of inflammatory T cell clones by providing cytokines that facilitate the disease process.
Original language | English |
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Pages (from-to) | 92-98 |
Number of pages | 7 |
Journal | Cellular Immunology |
Volume | 189 |
Issue number | 2 |
DOIs | |
State | Published - 1 Nov 1998 |
Keywords
- Diabetes transfer
- Islet-specific T cell clones
- NOD mouse