Potential role of major histocompatibility complex class II peptides in regulatory tolerance to vascularized grafts.
The inactivation of persisting T lymphocytes reactive to self- and non-self-antigens is a major arm of operational immune tolerance in mammals. Silencing of such T cells proceeds mostly by means of suppression, a process that is mediated by regulatory T-cell subsets and especially by CD4(+)CD(25high) regulatory T cells (Treg). Although Treg activation and ensuing suppressive activity appear to be major histocompatibility complex class II dependent, the fine specificity of Treg T-cell receptors has not yet been elucidated. Recent data from the author's laboratory on a class II gene therapy induction of tolerance to allogeneic kidney grafts suggest that class II peptides are involved as generic signals for Treg activation. A brief compilation of results that would support this hypothesis is discussed in the present article.
LeGuern
Christian
C
Transplantation Biology Research Center, Massachusetts General Hospital, Harvard Medical School, Boston, MA 02129, USA. leguern@helix.mgh.harvard.edu
D000818:Animals; D000949:Histocompatibility Antigens Class II / Q000502:physiology*; D006801:Humans; D016030:Kidney Transplantation; D010446:Peptide Fragments / Q000502:physiology; D012079:Renal Circulation; D013601:T-Lymphocytes / Q000502:physiology*; D023001:Transplantation Tolerance / Q000502:physiology*
D000949:Histocompatibility Antigens Class II; D010446:Peptide Fragments