Phenotypes Associated with This Genotype

Genotype
MGI:4360483

hm3

• Allelic Composition: Il1b^tm1Lvp/Il1b^tm1Lvp
• Genetic Background: involves: 129S7/SvEvBrd * C57BL/6

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

mortality/aging

decreased susceptibility to induced morbidity/mortality ( J:67001 )

• following acetylcholine receptor-induced clinical experimental autoimmune myasthenia gravis

immune system

abnormal lymphocyte physiology ( J:67001 )

• following acetylcholine receptor-induced clinical experimental autoimmune myasthenia gravis, popliteal and inguinal lymph node mononuclear cell proliferation is reduced compared to in similarly treated wild-type mice

• however, anti-CD3-induced T cell proliferation is normal

decreased circulating interleukin-1 beta level ( J:27234 )

• mice fail to produce IL-1 beta at a basal level or in response to LPS administration

decreased interferon-gamma secretion ( J:67001 )

• following acetylcholine receptor-stimulation of popliteal and inguinal lymph node mononuclear cells

decreased interleukin-2 secretion ( J:67001 )

• following acetylcholine receptor-stimulation of popliteal and inguinal lymph node mononuclear cells

decreased interleukin-4 secretion ( J:67001 )

• following acetylcholine receptor-stimulation of popliteal and inguinal lymph node mononuclear cells

abnormal interleukin-6 secretion ( J:27234 )

• mice fail to increase plasma levels of IL-6 in response to the turpentine injection

• in contrast, control mice have a peak of plasma IL-6 levels about 10-fold above basal 8 hours after injection with levels remaining above basal for at least 96 hours post-injection

decreased susceptibility to experimental autoimmune myasthenia gravis ( J:67001 )

• mice are resistant to acetylcholine receptor-induced clinical experimental autoimmune myasthenia gravis (decreased mortality, muscle weakness, lymphocyte proliferation, Th1 and Th2 cytokine production, and serum acetylcholine receptor antibodies) compared with similarly treated wild-type mice

decreased inflammatory response ( J:27234 )

• some of the long-term side effects of the inflammatory response to turpentine does not occur in these mice

• these side effects include loss of weight, decrease food and water intake

• influx of white blood cells to the injection site occurs in a manner similar to wild-type mice

decreased acute inflammation ( J:27234 )

• mice fail to develop a fever in response to the inflammatory agent turpentine

• mice also fail to increase plasma levels of IL-6 in response to the turpentine injection

• there is a 2- to 5- fold reduction in mRNA transcripts for acute-phase proteins after 8- to 72 hours after turpentine injection

homeostasis/metabolism

decreased circulating interleukin-1 beta level ( J:27234 )

• mice fail to produce IL-1 beta at a basal level or in response to LPS administration

impaired febrile response ( J:27234 )

• mice fail to develop a fever in response to the inflammatory agent turpentine

• in contrast, mice develop a fever starting 5 hours after administration that lasts for 24 hours

• control mice also have a decrease in locomotor activity the night after injection while mutant mice have normal activity

hematopoietic system

abnormal lymphocyte physiology ( J:67001 )

• following acetylcholine receptor-induced clinical experimental autoimmune myasthenia gravis, popliteal and inguinal lymph node mononuclear cell proliferation is reduced compared to in similarly treated wild-type mice

• however, anti-CD3-induced T cell proliferation is normal