Phenotypes Associated with This Genotype

Genotype
MGI:3039441

• Allelic Composition: Myd88^tm1Aki/Myd88^tm1Aki
• Genetic Background: Not Specified

• ♀: phenotype observed in females
• ♂: phenotype observed in males
• N: normal phenotype

cellular

decreased B cell proliferation ( J:96773 )

• splenocytes showed a defect in proliferation in response to the TLR4 ligand lipopolysaccharide (LPS), bacterial lipopeptide (BLP) that signals through the TLR1-TLR2 heterodimer, the TLR9 ligand unmethylated CpG DNA (CpG) and to the TLR7 ligand resiquimod (R-848)

immune system

decreased B cell proliferation ( J:96773 )

• splenocytes showed a defect in proliferation in response to the TLR4 ligand lipopolysaccharide (LPS), bacterial lipopeptide (BLP) that signals through the TLR1-TLR2 heterodimer, the TLR9 ligand unmethylated CpG DNA (CpG) and to the TLR7 ligand resiquimod (R-848)

abnormal NK cell physiology ( J:88906 )

• NK and NK-T cell activation is significantly lower compared to C57BL/6 wild-type controls during mouse cytomegalovirus infection

abnormal T cell physiology ( J:96773 )

• thymocytes failed to proliferate in response to IL-1

abnormal NK T cell physiology ( J:88906 )

• NK and NK-T cell activation is significantly lower compared to C57BL/6 wild-type controls during mouse cytomegalovirus infection

abnormal macrophage physiology ( J:96773 )

• activation of NF-kappaB, JNK, p38 and ERK in bone marrow derived macrophages was delayed in response to LPS and absent in response to BLP and CpG

abnormal dendritic cell physiology ( J:96773 )

• dendritic cells produced barely detectable amounts of cytokines in response to LPS or CpG

• dendritic cells mature only in response to LPS but not CpG

abnormal cytokine secretion ( J:88906 , J:89257 )

• type 1 IFN, IFNgamma and IL-12 p40 levels are decreased compared to C57BL/6 wild-type controls following sublethal viral infection (J:88906)

• IFNalpha was not secreted after infection with vesicular stomatitis virus (a ssRNA virus) (J:89257)

increased susceptibility to Herpesvirales infection ( J:88906 )

• viral loads and mortality are significantly higher after mouse cytomegalovirus infection compared to C57BL/6 wild-type controls

hematopoietic system

decreased B cell proliferation ( J:96773 )

• splenocytes showed a defect in proliferation in response to the TLR4 ligand lipopolysaccharide (LPS), bacterial lipopeptide (BLP) that signals through the TLR1-TLR2 heterodimer, the TLR9 ligand unmethylated CpG DNA (CpG) and to the TLR7 ligand resiquimod (R-848)

abnormal NK cell physiology ( J:88906 )

• NK and NK-T cell activation is significantly lower compared to C57BL/6 wild-type controls during mouse cytomegalovirus infection

abnormal T cell physiology ( J:96773 )

• thymocytes failed to proliferate in response to IL-1

abnormal NK T cell physiology ( J:88906 )

• NK and NK-T cell activation is significantly lower compared to C57BL/6 wild-type controls during mouse cytomegalovirus infection

abnormal macrophage physiology ( J:96773 )

• activation of NF-kappaB, JNK, p38 and ERK in bone marrow derived macrophages was delayed in response to LPS and absent in response to BLP and CpG