Defective Invariant Natural Killer T-Cell Suppression in Patients With Type 1 Diabetes
Defective Invariant Natural Killer T-Cell Suppression in Patients With Type 1 Diabetes
复制标题
1 型糖尿病患者的缺陷性恒定自然杀伤 T 细胞抑制
作者：
I. Nel;A. Lehuen
Type 1 diabetes (T1D) results from gradual alteration of insulin-secreting pancreatic β-cells. When most β-cells are destroyed and/or nonfunctional, patients are unable to regulate hyperglycemia and clinical signs appear (1). Although T cells play a key role in β-cell destruction, other immune cells are also involved in T1D physiopathology (2). Both Foxp3+ regulatory T cells (Tregs) and invariant natural killer T (iNKT) cells exert a major role in maintaining peripheral tolerance. iNKT cells are unconventional T lymphocytes expressing the semi-invariant T-cell receptor (Vα14-Jα18 in mice, Vα24-Jα18 in humans). They recognize glycolipid ligands, presented by the highly conserved CD1d molecule. iNKT cells are considered as “innate-like” T cells because they express a memory phenotype and rapidly respond upon activation. NOD mice, which spontaneously develop T1D, present abnormalities in iNKT cell frequency and function. Studies based on this mouse model have demonstrated the protective role of iNKT cells in T1D. Increasing iNKT cell frequency by adoptive transfer or Vα14-Jα18 transgenesis decreases T1D incidence (3,4). Conversely, CD1d-deficient NOD mice lacking iNKT cells present an acceleration of T1D development (5). Ligand-specific stimulation of iNKT cells suggests that the protective and regulatory role of these cells could be used as a therapeutic strategy in patients (6,7). Although numerous studies using mouse models have highlighted the regulatory role of iNKT cells in T1D, the regulatory role of iNKT cells in T1D patients remains unclear.
In this issue, Usero et al. (8) show for the first time in vitro that iNKT cell suppression of T-cell response is …
影响因子：
15.9
作者：
Kukreja, A;Cost, G;Maclaren, N
通讯作者：
Maclaren, N
影响因子：
30.3
作者：
Kostic AD;Gevers D;Siljander H;Vatanen T;Hyötyläinen T;Hämäläinen AM;Peet A;Tillmann V;Pöhö P;Mattila I;Lähdesmäki H;Franzosa EA;Vaarala O;de Goffau M;Harmsen H;Ilonen J;Virtanen SM;Clish CB;Orešič M;Huttenhower C;Knip M;DIABIMMUNE Study Group;Xavier RJ
通讯作者：
Xavier RJ