Table 2 Murine models of MCD Citation .... | American Society of Hematology

Table 2

Murine models of MCD

Citation	Murine model	Key findings
Brandt et al 1990⁴⁵	Congenitally anemic W/Wv mice reconstituted with bone marrow cells were transduced with a retroviral vector that introduced the coding sequences of murine IL-6 into mouse hematopoietic cells.	Mice demonstrated MCD features, including anemia, transient granulocytosis, hypoalbuminemia, plasma cell infiltration, and polyclonal hypergammaglobulinemia, with marked splenomegaly and peripheral lymphadenopathy
Screpanti et al 1995⁴⁷	C/EBPβ knockout mice were generated by gene targeting through homologous recombination at the endogenous C/EBPβ locus.	C/EBPβ^−/− mice develop a syndrome similar to mice overexpressing IL-6 and very similar to human MCD, with splenomegaly, lymphadenopathy, and enhanced hematopoiesis. There was also dysfunction of humoral, innate and cellular immunity, including defective activation of splenic macrophages, impaired IL-12 production, increased susceptibility to Candida albicans, and T-helper cell dysfunction.
Katsume et al 2002⁴⁶	Transgenic mice carrying human IL-6 cDNA fused with a murine major histocompatibility class I promoter were administered with an anti-IL-6 receptor antibody.	The untreated transgenic mice developed plasmacytosis, mesangial proliferative glomerulonephritis, leukocytosis, thrombocytosis, anemia, and other laboratory abnormalities. Treatment prevented all symptoms and extended the lifetime of most mice.

Citation	Murine model	Key findings
Brandt et al 1990⁴⁵	Congenitally anemic W/Wv mice reconstituted with bone marrow cells were transduced with a retroviral vector that introduced the coding sequences of murine IL-6 into mouse hematopoietic cells.	Mice demonstrated MCD features, including anemia, transient granulocytosis, hypoalbuminemia, plasma cell infiltration, and polyclonal hypergammaglobulinemia, with marked splenomegaly and peripheral lymphadenopathy
Screpanti et al 1995⁴⁷	C/EBPβ knockout mice were generated by gene targeting through homologous recombination at the endogenous C/EBPβ locus.	C/EBPβ^−/− mice develop a syndrome similar to mice overexpressing IL-6 and very similar to human MCD, with splenomegaly, lymphadenopathy, and enhanced hematopoiesis. There was also dysfunction of humoral, innate and cellular immunity, including defective activation of splenic macrophages, impaired IL-12 production, increased susceptibility to Candida albicans, and T-helper cell dysfunction.
Katsume et al 2002⁴⁶	Transgenic mice carrying human IL-6 cDNA fused with a murine major histocompatibility class I promoter were administered with an anti-IL-6 receptor antibody.	The untreated transgenic mice developed plasmacytosis, mesangial proliferative glomerulonephritis, leukocytosis, thrombocytosis, anemia, and other laboratory abnormalities. Treatment prevented all symptoms and extended the lifetime of most mice.