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MAdCAM‐1 is needed for diabetes development mediated by the T cell clone, BDC‐2·5
Author(s) -
Phillips Jenny M.,
Haskins Kathryn,
Cooke Anne
Publication year - 2005
Publication title -
immunology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.297
H-Index - 133
eISSN - 1365-2567
pISSN - 0019-2805
DOI - 10.1111/j.1365-2567.2005.02254.x
Subject(s) - clone (java method) , addressin , nod mice , nod , diabetes mellitus , adoptive cell transfer , immunology , pancreas , cd8 , type 1 diabetes , endocrinology , biology , medicine , t cell , immune system , cell , cell adhesion , genetics , gene
Summary The NOD‐derived islet‐reactive CD4 + T cell clone, BDC‐2·5, is able to transfer diabetes to neonatal non‐obese diabetic (NOD) mice but is unable to transfer disease to either adult NOD or NOD scid recipients. Transfer of diabetes to adult recipients by BDC‐2·5 is only accomplished by cotransfer of CD8 + T cells from a diabetic donor. To understand why this CD4 + T cell clone is able to mediate diabetes in neonatal but not the adult recipients we examined the ability of the clone to traffic in the different recipients. Our studies showed that MAdCAM‐1 has a very different expression pattern in the neonatal and adult pancreas. Blockade of this addressin prevents the clone from transferring diabetes to neonatal mice, suggesting that the differential pancreatic expression of MAdCAM‐1 in neonatal and adult pancreas provides an explanation of the differences in diabetes development.