Despite its potent action on hematopoietic progenitor cell development in vitro, mice with a targeted disruption of the IL-11 receptor-a (IL-11Ra) had normal baseline hematopoiesis, immune function, and erythroid reserves (75) but displayed a defect in postimplantation decidualization that impaired the fertility of female mice (76). Mice deficient in gp130, the partner of IL-11-Ra in the heterodimeric IL-11 receptor, display additional defects that reflect defective signaling from other ligands that share gp130 as a component of their heterodimeric receptors: IL-6, leukemia inhibitory factor (LIF), ciliary neurotropic growth factor (CNTF), oncostatin M, and cardiotropin (CT). Absolute gp130 deficiency results in embryonic lethality from multiple defects including impaired fetal liver hematopoiesis (71). When embryonic lethality was circumvented by a genetically based inducible Cre-lox gene targeting approach, adult gp130-deficient mice developed multisystem defects including thrombocytopenia, leukocytosis, and impaired hematopoietic recovery after 5-fluorouracil (5-FU) stem-cell ablation or after antiplatelet antiserum (77).

IL-11 has been neutralized in mice by passive immunization using a sheep anti-MuIL-11 Ab in a study investigating the role of IL-11 in bone changes after oophorectomy (78).

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