title: Interleukin-2 is indispensable for development of immunological self-tolerance.
abstract: Interleukin-2-deficient mice (IL-2(-/-)) manifest severe immune system abnormalities characterized by an uncontrolled activation and proliferation of lymphocytes. A systemic autoimmune syndrome results, and hemolytic anemia leads to early death especially in mice derived from a BALB/c genotype. Remarkably, IL-2 treatment prevents both the activation of the immune system and the development of autoimmune disease. Moreover, adoptive transfer of lymphocytes from IL-2-treated IL-2(-/-) animals confers protection to IL-2(-/-) mice, suggesting that IL-2 induces a postnatal differentiation/maturation of regulatory cells necessary for self- and non-self-discrimination.
authors.affiliation: Institute of Virology and Immunobiology, University of Würzburg, Germany.
authors.forename: G
authors.initials: G
authors.lastname: Klebb
authors.forename: I B
authors.initials: IB
authors.lastname: Autenrieth
authors.forename: H
authors.initials: H
authors.lastname: Haber
authors.forename: E
authors.initials: E
authors.lastname: Gillert
authors.forename: B
authors.initials: B
authors.lastname: Sadlack
authors.forename: K A
authors.initials: KA
authors.lastname: Smith
authors.forename: I
authors.initials: I
authors.lastname: Horak
mesh_terms: D000744:Anemia, Hemolytic, Autoimmune / Q000276:immunology / Q000517:prevention & control; D000818:Animals; D003433:Crosses, Genetic; D004195:Disease Models, Animal; D007376:Interleukin-2 / Q000502:physiology* / Q000627:therapeutic use; D051379:Mice; D008807:Mice, Inbred BALB C; D008810:Mice, Inbred C57BL; D017634:Self Tolerance
chemical_list: D007376:Interleukin-2