hematopoietic system phenotype

• abnormal CD8-positive, alpha-beta T cell physiology
  • 7 days after immunization of mutant mice with OVA-loaded Tap1-null cells, stimulation of splenocytes with OVA peptide revealed a 3- to 4-fold reduction in generation of OVA-specific CD8+ T cells responses in vivo
  (MGI Ref ID J:122479)

• abnormal lymphocyte physiology
  • decay of surface K^b and d^b molecules on brefeldin A-treated cells is increased compared to wild-type, but is less pronounced than on Tapbp-null treated cells
  (MGI Ref ID J:122479)

mammalian phenotype

• immune system phenotype
  • null mice show insignificant differences in response to infection with an influenza virus
  (MGI Ref ID J:122479)
  • CD8+ T cell development is normal in homozygous mice
  (MGI Ref ID J:122479)

immune system phenotype

• abnormal antigen presentation
  • a panel of Qa-1^b-restricted, alloreactive CTL clones each show a significant reduction in capacity to lyse mutant splenic cells compared with wild-type cells
  (MGI Ref ID J:122479)
  • dendritic cells infected with LCMV show enhanced reactivity with gp33 (immunodominant LCMV-derived epitope)-T cells compared to wild-type cells
  (MGI Ref ID J:122479)
  • defective presentation of self-antigens to class I-restricted cytotoxic T lymphocytes (CTLs) is observed in null-cells; defects in reactivity of two H60-specific CTL clones and an HY-specific clone with null cells is seen, while H4^b-specific clones react similarly with null splenocytes and wild-type cells, and an H13^b-specific clone reacted with null cells more strongly than with wild-type
  (MGI Ref ID J:122479)
  • ic H-2K^b-restricted T cell hybridoma
  (MGI Ref ID J:122479)
  • when ovalbumin is introduced to cell cytoplasm by osmotic shock, mutant cells show impairment in presentation of OVA-derived epitopes; bone marrow-derived dendritic cells and LPS-induced lymphoblasts are also defective in presenting OVA to a an OVA-specific H-2K^b-restricted T cell hybridoma
  (MGI Ref ID J:122479)
  • mutant macrophages infected with OVA-expressing bacteria are defective in antigen presentation to OVA specific T cells
  (MGI Ref ID J:122479)
  • ones react similarly with null splenocytes and wild-type cells, and an H13^b-specific clone reacted with null cells more strongly than with wild-type
  (MGI Ref ID J:122479)

• increased level of surface class I molecules
  (MGI Ref ID J:122479)

• decreased level of surface class I molecules
  • reduction in surface expression of H-2K^b and H-2D^b molecules on total mononuclear cells in spleen, lymph node, and blood including splenic dendritic cells, T cells, and B cells, as well as fibroblast cell lines from mice
  (MGI Ref ID J:122479)
  • levels of H-2K^b and H-2D^b are reduced ~40 and 50% respectively; extent of surface display of nonclassical class I molecule Qa-2 is reduced ~35% compared to wild-type cells
  (MGI Ref ID J:122479)

• abnormal CD8-positive, alpha-beta T cell physiology
  • 7 days after immunization of mutant mice with OVA-loaded Tap1-null cells, stimulation of splenocytes with OVA peptide revealed a 3- to 4-fold reduction in generation of OVA-specific CD8+ T cells responses in vivo
  (MGI Ref ID J:122479)

• abnormal lymphocyte physiology
  • decay of surface K^b and d^b molecules on brefeldin A-treated cells is increased compared to wild-type, but is less pronounced than on Tapbp-null treated cells
  (MGI Ref ID J:122479)

immune system phenotype

• decreased level of surface class I molecules
  • heterozygous animals show intermediate expression levels of class I molecules between homozygotes and wild-type mice
  (MGI Ref ID J:122479)

• abnormal antigen presentation
  • heterozygous cells show impairment in processing OVA for surface display by K^b
  (MGI Ref ID J:122479)