Abstract:
:Invariant CD1d-restricted natural killer T (iNKT) cells function during innate and adaptive immune responses. A functional and numerical deficiency of iNKT cells is well documented in both nonobese diabetic (NOD) mice and humans with autoimmune type 1 diabetes (T1D). Restoring the numerical and/or functional deficiency of iNKT cells in NOD mice by either treatment with alpha-galactosylceramide, transgenic induction of Valpha14-Jalpha18 expression, or transgenic expression of CD1d in NOD islets under the control of the human insulin promoter confers protection from T1D in these mice. Recently, considerable progress has been made in understanding the developmental and functional activities of iNKT cells. In this review, we discuss the role of iNKT cell deficiency and defective development in the onset of T1D in NOD mice and the different protective mechanisms known to restore these defects.
journal_name
Immunol Resjournal_title
Immunologic researchauthors
Hussain S,Wagner M,Ly D,Delovitch TLdoi
10.1385/IR:31:3:177subject
Has Abstractpub_date
2005-01-01 00:00:00pages
177-88issue
3eissn
0257-277Xissn
1559-0755pii
IR:31:3:177journal_volume
31pub_type
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