Phenotypes Associated with This Genotype

Genotype
MGI:3587743

• Allelic Composition: Ifng^tm1Ts/Ifng^tm1Ts
• Genetic Background: involves: 129S7/SvEvBrd * C57BL/6

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

immune system

immune system phenotype ( J:119206 )

N • mice are able to clear infections of Pneumocystis carinii, similar to controls

increased splenocyte proliferation ( J:66802 )

• splenocytes from BCG infected mice exhibit increased proliferation in response to Con A

abnormal NK cell physiology ( J:66802 , J:115033 )

• significantly lower resting splenic NK cell activity (J:66802)

• recruitment of NK cells to the liver by recombinant murine IL12 is impaired (J:115033)

• however, the recruitment of T cells by IL12 is not impaired (J:115033)

abnormal macrophage physiology ( J:66802 )

• macrophages from BCG infected mice fail to produce nitric oxide in response to LPS challenge

• macrophages from BCG infected mice exhibit reduced production of superoxide anion in response to PMA challenge

abnormal MHC II cell surface expression on macrophages ( J:66802 )

• macrophages from BCG infected mice exhibit reduced class II expression

abnormal type IV hypersensitivity reaction ( J:55740 )

• exposure to UVA and UVB fails to significantly reduce the UVB induced suppression of the type IV hypersensitivity reaction

• however, the type IV hypersensitivity reaction in the absence of UV exposure is similar to controls

increased susceptibility to bacterial infection ( J:66802 )

• increased mortality following a sublethal dose of Mycobacterium bovis (BCG )

decreased susceptibility to parasitic infection ( J:189794 )

• mice infected with Plasmodium berghei ANKA are protected from development of experimental cerebral malaria and survive longer than wild-type mice

• however, IFNG-competent alpha+CD4+ T cells promote experimental cerebral malaria

decreased susceptibility to parasitic infection induced morbidity/mortality ( J:189794 )

• mice infected with Plasmodium berghei ANKA are protected from development of experimental cerebral malaria and survive longer than wild-type mice

decreased length of allograft survival ( J:44346 )

• reduced surival of cardiac grafts relative to controls

growth/size/body

alveolar process atrophy ( J:147935 )

• modest increase in alveolar bone loss at 30 weeks relative to mice at 6 and 16 weeks

neoplasm

increased metastatic potential ( J:152785 )

• following treatment with alphaGalCer, mice fail to exhibit a reduction in the number of B16F10 tumors metastasizing to the lungs unlike similarly treated wild-type mice

decreased tumor incidence ( J:138466 )

• tumor-bearing mice treated with Th-17-polarized cells from Tg(Tcra,Tcrb)9Rest cells show increased tumor rejection compared to controls

craniofacial

alveolar process atrophy ( J:147935 )

• modest increase in alveolar bone loss at 30 weeks relative to mice at 6 and 16 weeks

skeleton

alveolar process atrophy ( J:147935 )

• modest increase in alveolar bone loss at 30 weeks relative to mice at 6 and 16 weeks

hematopoietic system

increased splenocyte proliferation ( J:66802 )

• splenocytes from BCG infected mice exhibit increased proliferation in response to Con A

abnormal NK cell physiology ( J:66802 , J:115033 )

• significantly lower resting splenic NK cell activity (J:66802)

• recruitment of NK cells to the liver by recombinant murine IL12 is impaired (J:115033)

• however, the recruitment of T cells by IL12 is not impaired (J:115033)

abnormal macrophage physiology ( J:66802 )

• macrophages from BCG infected mice fail to produce nitric oxide in response to LPS challenge

• macrophages from BCG infected mice exhibit reduced production of superoxide anion in response to PMA challenge

abnormal MHC II cell surface expression on macrophages ( J:66802 )

• macrophages from BCG infected mice exhibit reduced class II expression

integument

abnormal skin physiology ( J:55740 )

• following exposure to UVA and UVB mice fail to develop significant erythema unlike wild-type controls

• however, the increase in skin fold thickness in response to UVB or UVA and UVB exposure is not significantly different from controls

cellular

increased splenocyte proliferation ( J:66802 )

• splenocytes from BCG infected mice exhibit increased proliferation in response to Con A

mortality/aging

decreased susceptibility to parasitic infection induced morbidity/mortality ( J:189794 )

• mice infected with Plasmodium berghei ANKA are protected from development of experimental cerebral malaria and survive longer than wild-type mice

Mouse Models of Human Disease		DO ID	OMIM ID(s)	Ref(s)
malaria		DOID:12365		J:189794