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L-Selectin Is Not Required for T Cell-Mediated Autoimmune Diabetes¹

Randall H. Friedline^*, Carmen P. Wong^*, Douglas A. Steeber, Thomas F. Tedder and Roland Tisch^2,*

^* Department of Microbiology and Immunology, School of Medicine, University of North Carolina, Chapel Hill, NC 27599; and Department of Immunology, Duke University Medical Center, Durham, NC 27710

Administration of anti-L-selectin (CD62L) mAb to neonatal nonobese diabetic (NOD) mice mediates long term protection against the development of insulitis and overt diabetes. These results suggested that CD62L has a key role in the general function of cell-specific T cells. To further examine the role of CD62L in the development of type 1 diabetes, NOD mice lacking CD62L were established. The onset and frequency of overt diabetes were equivalent among CD62L^+/+, CD62L^+/-, and CD62L^-/- NOD littermates. Furthermore, patterns of T cell activation, migration, and cell-specific reactivity were similar in NOD mice of all three genotypes. Adoptive transfer experiments with CD62L^-/- CD4⁺ T cells prepared from BDC2.5 TCR transgenic mice revealed no apparent defects in migration to pancreatic lymph nodes, proliferation in response to cell Ag, or induction of diabetes in NOD.scid recipients. In conclusion, CD62L expression is not essential for the development of type 1 diabetes in NOD mice.

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