First Author | Peterson JD | Year | 1998 |
Journal | Cell Immunol | Volume | 189 |
Issue | 2 | Pages | 92-8 |
PubMed ID | 9790722 | Mgi Jnum | J:50793 |
Mgi Id | MGI:1309731 | Doi | 10.1006/cimm.1998.1377 |
Citation | Peterson JD, et al. (1998) Analysis of leukocytes recruited to the pancreas by diabetogenic T cell clones. Cell Immunol 189(2):92-8 |
abstractText | 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 Vbeta4(+)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 Vbeta monoclonal antibodies. The majority of the diabetes-initiating, Vbeta4(+) T cell clones migrated to the spleen whereas only 5-8% of the T cell population infiltrating the pancreas was Vbeta4(+). 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-gamma 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. Copyright 1998 Academic Press. |