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Characteristics of Rat CD4 + CD25 + T Cells and Their Ability to Prevent Not Only Diabetes But Also Insulitis in an Adoptive Transfer Model in BB Rats
Author(s) -
Holm T. L.,
Lundsgaard D.,
Markholst H.
Publication year - 2006
Publication title -
scandinavian journal of immunology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.934
H-Index - 88
eISSN - 1365-3083
pISSN - 0300-9475
DOI - 10.1111/j.1365-3083.2006.01760.x
Subject(s) - insulitis , il 2 receptor , foxp3 , adoptive cell transfer , lymph , cd80 , endocrinology , biology , t cell , medicine , immunology , immune system , diabetes mellitus , in vitro , cytotoxic t cell , type 1 diabetes , pathology , cd40 , biochemistry
Human and mouse CD4 + CD25 + T cells have been intensively studied through the last decade. However, little is known about this subset in other species. This study describes the phenotype of rat CD4 + CD25 + Foxp3 + T cells and the site in which they exert regulation in a transfer‐induced autoimmune diabetes model. Several proteins and mRNAs are up‐regulated in unstimulated rat CD4 + CD25 + T cells compared with CD4 + CD25 – T cells, including Foxp3, Lag‐3, CD80, interleukin 10 (IL‐10) and CTLA‐4. To investigate CD4 + CD25 + T cells in vivo , we transferred three million diabetogenic T cells either alone or in combination with two million CD4 + CD25 + T cells to 30‐day‐old BB rats. The pancreas and the pancreatic lymph nodes were examined as two potential regulatory sites. Time‐course analysis of pancreatic histology following diabetogenic T‐cell transfers revealed insulitis from about 14 days after transfer. By contrast, rats receiving both diabetogenic T cells and CD4 + CD25 + T cells had no insulitis at any time. Moreover, the frequency of diabetogenic T cells in the pancreatic lymph nodes 2 days after transfer was significantly reduced in rats receiving both subsets. These data indicate that the primary site of T‐cell regulation is in the draining lymph nodes and not the pancreas in our model.