@Article{,
AUTHOR = {Elena Voronov, Molly Dayan, Heidy Zinger, Lubov Gayvoronsky, Jian-Ping Lin, Yoichiro Iwakura, Ron N. Apte, Edna Mozes},
TITLE = {IL-1β-deficient mice are resistant to induction of experimental SLE},
JOURNAL = {European Cytokine Network},
VOLUME = {17},
YEAR = {2006},
NUMBER = {2},
PAGES = {109--116},
URL = {http://www.techscience.com/ECN/v17n2/66156},
ISSN = {1952-4005},
ABSTRACT = {IL-1 is one of the most pleiotropic pro-inflammatory and immunostimulatory cytokines. Overproduction
of IL-1 has been shown to be involved in the pathogenicity of various autoimmune inflammatory diseases,
including systemic lupus erythematosus (SLE). However, the different contributions that the IL-1 agonistic
molecules make in their in vivo native milieu, IL-1β which is mainly secreted against IL-1α which is mainly
cell-associated, have not been established. Experimental SLE can be induced in mice by injection with monoclonal
anti-DNA antibodies bearing a major idiotype designated, 16/6Id. In the present study, experimental SLE was
induced in mice deficient in specific IL-1 molecules, i.e. IL-1α<sup>-/-</sup>, IL-1β<sup>-/-</sup>, IL-1α/β<sup>-/-</sup> (double KO) and in control
BALB/c mice. Mice deficient in IL-1β, i.e. IL-1β<sup>-/-</sup> and IL-1α/β<sup>-/-</sup> mice, developed lower levels of anti-dsDNA
antibodies after immunization with 16/6Id, as compared to IL-1α<sup>-/-</sup> or control BALB/c mice. Disease manifestations
were milder in mice deficient in IL-1β expression. The representative cytokine cascade that is characteristic
of overt experimental SLE was also shown to be reduced in groups of mice that lacked IL-1β as compared to mice
deficient in IL-1α, which is mainly cell-associated. Altogether, our results point to the importance of secretable
IL-1β, rather than cell-associated IL-1α, in the immunostimulatory and inflammatory phenomena that mediate
the pathogenesis of experimental SLE.},
DOI = {}
}