Interleukin-2 is indispensable for development of immunological self-tolerance.
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.
Klebb
G
G
Institute of Virology and Immunobiology, University of Würzburg, Germany.
Autenrieth
I B
IB
Haber
H
H
Gillert
E
E
Sadlack
B
B
Smith
K A
KA
Horak
I
I
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
D007376:Interleukin-2