digestive/alimentary system
• a few apoptotic cells are seen in the inflammatory lesions of salivary glands indicating destruction of salivary glands
|
• amount of saliva collected from mutants is lower than from wild-type mice at 8 and 12 weeks of age, but not at 3 weeks
|
• mononuclear cells are seen infiltrating the salivary glands
• most infiltrating cells in the salivary gland are CD3+ T (mainly CD4+ T) cells and B cells gradually increase in number with age and most infiltrating cells at later states are B cells
|
nervous system
• Theilers murine encephalomyelitis virus (TMEV) infected mice develop a demyelinating disease 2-3 months after infection that is not seen in infected wild-type mice
• viral antigen positive cells are seen around demyelinating lesions of TMEV-infected mice
|
immune system
• mononuclear cells are seen infiltrating the salivary glands
• most infiltrating cells in the salivary gland are CD3+ T (mainly CD4+ T) cells and B cells gradually increase in number with age and most infiltrating cells at later states are B cells
|
• mononuclear cells are seen infiltrating the lacrimal glands
|
• mice have reduced CD8+ T cell numbers and enhanced IL-17 production during the acute phase of TMEV infection
• TMEV-infected mice show a decrease in the number of IFN-gamma secreting CD8+ T cells
|
• TMEV-infected mice have a higher percentage of IL-17+ cells among CD4+ T cells at 1 week post infection
|
• reduction in the number of CD4+CD25+Foxp3+ Treg cells in the thymus, spleen, and cervical lymph nodes
|
• CD4+ T cells in the spleen, cervical lymph nodes, and salivary glands are mainly effector memory cells
|
• mice infected with TMEV show slightly less anti-TMEV IgG responses than wild-type mice at 2 months post infection
|
• mice infected with TMEV have less anti-TMEV IgG2c in the serum than wild-type mice
|
• mice infected with TMEV have less anti-TMEV IgG3 in the serum than wild-type mice
|
• mice have enhanced TMEV-specific Th17 immune responses during the chronic phase of TMEV infection
• TMEV-infected mice have enhanced Th17 immune responses in the CNS during the acute stage of infection
|
• isolated MNCs stimulated with TMEV produce less IFN-gamma than wild-type MNCs
|
• spleen MNCs secrete more IFN-gamma at 1 week post TMEV infection than wild-type MNCs
• higher levels of IFN-gamma are seen in the spinal cord of TMEV-infected mice at 2 months post infection
|
• isolated MNCs stimulated with TMEV produce more less IL-10 than wild-type MNCs
|
• isolated MNCs stimulated with TMEV produce more IL-17 than wild-type MNCs
• spleen MNCs secrete more IL-17 at 1 week post TMEV infection than wild-type MNCs
• spinal cords from TMEV-infected mice show higher levels of IL-17 at 2 months post infection
|
• mice develop autoimmune sialadenitis-like Sjogrens Syndrome
• expression analysis of salivary gland lesions indicate the involvement of Th17, Th1, Th2, and Tfh cells in sialadenitis
|
• mice show higher levels of anti-M3R and anti-Sjogrens syndrome type A (SSA) antibodies in sera and a trend toward increased anti-Sjogrens syndrome type B (SSB) antibodies
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• trend toward increased anti-ANA antibodies
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• mild mononuclear cell infiltration in lungs
|
• mice infected with the Daniels strain of Theilers murine encephalomyelitis virus (TMEV) develop an acute CNS disease similar to infected wild-type mice, showing similar incidence of seizures, and amounts of inflammation and neural death in the CNS, however they do not resolve the infection as in wild-type mice and develop Theilers murine encephalomyelitis virus-induced demyelinating disease (TMEV-IDD) with severe inflammatory demyelinating lesions in the spinal cord 2-3 months after infection
• inflammatory cells of TMEV-infected mice are primarily mononuclear cells (MNCs) and the majority of inflammatory cells in the spinal cord are CD3+
• TMEV-infected mice have more viral RNA in the CNS than wild-type mice at 1 week post infection
|
endocrine/exocrine glands
• a few apoptotic cells are seen in the inflammatory lesions of salivary glands indicating destruction of salivary glands
|
• amount of saliva collected from mutants is lower than from wild-type mice at 8 and 12 weeks of age, but not at 3 weeks
|
• mononuclear cells are seen infiltrating the salivary glands
• most infiltrating cells in the salivary gland are CD3+ T (mainly CD4+ T) cells and B cells gradually increase in number with age and most infiltrating cells at later states are B cells
|
• mononuclear cells are seen infiltrating the lacrimal glands
|
homeostasis/metabolism
• amount of saliva collected from mutants is lower than from wild-type mice at 8 and 12 weeks of age, but not at 3 weeks
|
hematopoietic system
• mice have reduced CD8+ T cell numbers and enhanced IL-17 production during the acute phase of TMEV infection
• TMEV-infected mice show a decrease in the number of IFN-gamma secreting CD8+ T cells
|
• TMEV-infected mice have a higher percentage of IL-17+ cells among CD4+ T cells at 1 week post infection
|
• reduction in the number of CD4+CD25+Foxp3+ Treg cells in the thymus, spleen, and cervical lymph nodes
|
• CD4+ T cells in the spleen, cervical lymph nodes, and salivary glands are mainly effector memory cells
|
• mice infected with TMEV show slightly less anti-TMEV IgG responses than wild-type mice at 2 months post infection
|
• mice infected with TMEV have less anti-TMEV IgG2c in the serum than wild-type mice
|
• mice infected with TMEV have less anti-TMEV IgG3 in the serum than wild-type mice
|
• mice have enhanced TMEV-specific Th17 immune responses during the chronic phase of TMEV infection
• TMEV-infected mice have enhanced Th17 immune responses in the CNS during the acute stage of infection
|
respiratory system
• mild mononuclear cell infiltration in lungs
|
behavior/neurological
N |
• although TMEV-infected mice develop inflammatory demyelination 2-3 months after infection, they do not show weight loss, waddling gait, or impaired righting reflex
|
vision/eye
• mononuclear cells are seen infiltrating the lacrimal glands
|
Mouse Models of Human Disease |
DO ID | OMIM ID(s) | Ref(s) | |
Sjogren's syndrome | DOID:12894 |
OMIM:270150 |
J:230700 |