Horak I
Institute of Virology and Immunobiology, University of Würzburg, Germany.
Clin Immunol Immunopathol. 1995 Sep;76(3 Pt 2):S172-3. doi: 10.1016/s0090-1229(95)90126-4.
Interleukin-2-deficient mice (IL-2-/-) generated by targeted mutagenesis proved to be an excellent system to study the function of this lymphokine in the context of whole immune system. In addition, they provide an animal model of a primary immunodeficiency caused by a single-gene defect. Our results indicate that the essential degect in IL-2-/- mice is the lack of a negative regulatory function, which leads to breakdown of self tolerance. The development of autoimmune diseases in IL-2-deficient mice stresses the link between autoimmunity and primary immunodeficiencies.