mortality/aging
• following induction of experimental autoimmune encephalomyelitis
|
vision/eye
• mice show numerous white/yellow fundus lesions at 16 months of age but not at 3 months
|
• marker analysis indicates that photoreceptor maturation is abnormal with impaired outer segment elongation
|
• overall cilium structure is unaffected, however cilium proteins show altered distribution in the transitional zone during photoreceptor maturation
|
• cone number is reduced from P30 in the periphery and in the central retina at P90
• however, outer nuclear layer thickness is not altered in either the peripheral or central retina
|
• mice show shortened outer segments in P21 retina
|
• from P30 on
|
• microglial processes are often seen extending deep into the outer nuclear layer where photoreceptors reside
|
• cell loss is seen in the outer nuclear layer of 16 month old retina but not 3 month old retina
|
• late-stage retinal degeneration
|
• retina shows increased Muller cell gliosis from around eye opening at P14, becoming significant from 1 month of age, and extensive gliosis, particularly within the inner plexiform layer at 3 months of age
|
• 22% decrease in amplitude of the a-wave at P270 but not earlier, indicating a late onset of reduced rod-related function
|
• cone-related function is reduced from P17, shows no increase in response coincident with photoreceptor maturation, the functional deficit remains at P30 and P90, while no difference is seen at P270, with a decrease in b wave amplitude at P17, P30, and P90
|
nervous system
• following induction of experimental autoimmune encephalomyelitis
|
• following LPS exposure, neuron apoptosis is increased unlike in heterozygous mice
• LPS-induced neurotoxicity is cell-autonomous
• however, mice subjected to adoptive transfer experiments and treated with an IL1 receptor antagonist exhibit reduced neuron apoptosis
• however, adoptive transfer into Il1r null mice abolishes neuron apoptosis
|
• mice treated with 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) exhibit more severe neurotoxicity than similarly treated wild-type mice
|
• increase in microglia numbers in the outer nuclear layer from P14 and a trend for increased microglial process number from P14 becoming significant at P90
• presence of microglial processes in the outer retinal is increased at P14 compared with P90, with levels further increased at P270
• microglia at the level of the photoreceptor terminals exhibit normal soma size and process number with increased process length, indicating that microglia are not classically activated
|
microgliosis
(
J:110266
)
• intense and widespread following LPS exposure
|
• migration of microglial cells in LPS-treated mice is impaired unlike in similarly treated heterozygous mice
(J:110266)
• however, adoptive transfer into Il1r null mice restores microglial cell migration
(J:110266)
• microglial-cone interactions are increased in the central and peripheral retina at P21
(J:265696)
|
• following induction of experimental autoimmune encephalomyelitis
|
• marker analysis indicates that photoreceptor maturation is abnormal with impaired outer segment elongation
|
• overall cilium structure is unaffected, however cilium proteins show altered distribution in the transitional zone during photoreceptor maturation
|
• cone number is reduced from P30 in the periphery and in the central retina at P90
• however, outer nuclear layer thickness is not altered in either the peripheral or central retina
|
• mice show shortened outer segments in P21 retina
|
• from P30 on
|
• following induction of experimental autoimmune encephalomyelitis, mice exhibit more severe demyelination compared with similarly treated wild-type mice
|
immune system
N |
• mice exhibit normal response to murine cytomegalovirus infection
|
• in the central nervous system following induction of experimental autoimmune encephalomyelitis
|
• increase in microglia numbers in the outer nuclear layer from P14 and a trend for increased microglial process number from P14 becoming significant at P90
• presence of microglial processes in the outer retinal is increased at P14 compared with P90, with levels further increased at P270
• microglia at the level of the photoreceptor terminals exhibit normal soma size and process number with increased process length, indicating that microglia are not classically activated
|
microgliosis
(
J:110266
)
• intense and widespread following LPS exposure
|
• following arterial injury, monocyte recruitment is impaired compared to in similarly treated wild-type mice
|
• following induction of experimental autoimmune encephalomyelitis, recruitment of NK cells is impaired compared to in similarly treated wild-type mice
|
• migration of microglial cells in LPS-treated mice is impaired unlike in similarly treated heterozygous mice
(J:110266)
• however, adoptive transfer into Il1r null mice restores microglial cell migration
(J:110266)
• microglial-cone interactions are increased in the central and peripheral retina at P21
(J:265696)
|
• following induction of experimental autoimmune encephalomyelitis, mice exhibit earlier onset, higher mortality, and more severe EAE symptoms (nonremitting spastic paralysis, increased hemorrhagic inflammation, and extensive demyelination) compared with similarly treated wild-type mice
• following induction of experimental autoimmune encephalomyelitis, recruitment of NK cells is impaired compared to in similarly treated wild-type mice
• however, priming of encephalitogenic T cells and NKT cell numbers are normal
|
• following induction of experimental autoimmune encephalomyelitis
|
cardiovascular system
• following induction of experimental autoimmune encephalomyelitis
|
• following arterial injury, vascular smooth muscle cell proliferation is decreased compared to in similarly treated wild-type mice
• in vitro, vascular smooth muscle cells fail to proliferate in response to CXCL1 unlike similarly treated wild-type cells
|
• following arterial injury, mice exhibit decreased intimal hyperplasia, impaired monocyte recruitment into the vascular wall, and decreased vascular smooth muscle cell proliferation compared to in similarly treated wild-type mice
• however, mice exhibit normal luminal and medial areas and platelet function
|
homeostasis/metabolism
• following arterial injury, mice exhibit decreased intimal hyperplasia, impaired monocyte recruitment into the vascular wall, and decreased vascular smooth muscle cell proliferation compared to in similarly treated wild-type mice
• however, mice exhibit normal luminal and medial areas and platelet function
|
• mice treated with 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) exhibit more severe neurotoxicity than similarly treated wild-type mice
|
behavior/neurological
• following induction of experimental autoimmune encephalomyelitis, mice exhibit nonremitting spastic paralysis
|
hematopoietic system
• in the central nervous system following induction of experimental autoimmune encephalomyelitis
|
• increase in microglia numbers in the outer nuclear layer from P14 and a trend for increased microglial process number from P14 becoming significant at P90
• presence of microglial processes in the outer retinal is increased at P14 compared with P90, with levels further increased at P270
• microglia at the level of the photoreceptor terminals exhibit normal soma size and process number with increased process length, indicating that microglia are not classically activated
|
microgliosis
(
J:110266
)
• intense and widespread following LPS exposure
|
• following arterial injury, monocyte recruitment is impaired compared to in similarly treated wild-type mice
|
• following induction of experimental autoimmune encephalomyelitis, recruitment of NK cells is impaired compared to in similarly treated wild-type mice
|
• migration of microglial cells in LPS-treated mice is impaired unlike in similarly treated heterozygous mice
(J:110266)
• however, adoptive transfer into Il1r null mice restores microglial cell migration
(J:110266)
• microglial-cone interactions are increased in the central and peripheral retina at P21
(J:265696)
|
muscle
• following arterial injury, vascular smooth muscle cell proliferation is decreased compared to in similarly treated wild-type mice
• in vitro, vascular smooth muscle cells fail to proliferate in response to CXCL1 unlike similarly treated wild-type cells
|
cellular
• following arterial injury, vascular smooth muscle cell proliferation is decreased compared to in similarly treated wild-type mice
• in vitro, vascular smooth muscle cells fail to proliferate in response to CXCL1 unlike similarly treated wild-type cells
|
• overall cilium structure is unaffected, however cilium proteins show altered distribution in the transitional zone during photoreceptor maturation
|
• following LPS exposure, neuron apoptosis is increased unlike in heterozygous mice
• LPS-induced neurotoxicity is cell-autonomous
• however, mice subjected to adoptive transfer experiments and treated with an IL1 receptor antagonist exhibit reduced neuron apoptosis
• however, adoptive transfer into Il1r null mice abolishes neuron apoptosis
|
• mice treated with 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) exhibit more severe neurotoxicity than similarly treated wild-type mice
|