Phenotypes associated with this allele
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Find Mice |
Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Selltm1Pest mutation
(0 available);
any
Sell mutation
(41 available)
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immune system
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• in untreated Sell-deficient mice, WBCs do not experience activation-dependent LFA-1 mediated arrest and adhere to high endothelial venules (HEV)
• infusion of activated platelets restores rolling capability in Sell-deficient WBCs and greater than 50% become stably adherent to HEV
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• fraction of rolling Sell-deficient lymphocytes (12.1%) is reduced compared to wild-type littermates (72.1%)
• injection of activated, but not resting, human platelets enhanced rolling fraction to 48.9%, approaching a similar level to wild-type
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• lymph node T cells from sensitized platelet-treated mutant mice proliferate comparably to wild-type in response to antigen while T cells from untreated sensitized mutants do not proliferate at all
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• when mutant mice are sensitized to the antigen DFNB by topical application to abdominal skin and injected with activated human platelets, a dramatic contact hypersensitivity response is elicited 5 days later, compared to no response in sham-treated sensitized mutants
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hematopoietic system
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• in untreated Sell-deficient mice, WBCs do not experience activation-dependent LFA-1 mediated arrest and adhere to high endothelial venules (HEV)
• infusion of activated platelets restores rolling capability in Sell-deficient WBCs and greater than 50% become stably adherent to HEV
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• fraction of rolling Sell-deficient lymphocytes (12.1%) is reduced compared to wild-type littermates (72.1%)
• injection of activated, but not resting, human platelets enhanced rolling fraction to 48.9%, approaching a similar level to wild-type
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• lymph node T cells from sensitized platelet-treated mutant mice proliferate comparably to wild-type in response to antigen while T cells from untreated sensitized mutants do not proliferate at all
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cellular
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• in untreated Sell-deficient mice, WBCs do not experience activation-dependent LFA-1 mediated arrest and adhere to high endothelial venules (HEV)
• infusion of activated platelets restores rolling capability in Sell-deficient WBCs and greater than 50% become stably adherent to HEV
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• fraction of rolling Sell-deficient lymphocytes (12.1%) is reduced compared to wild-type littermates (72.1%)
• injection of activated, but not resting, human platelets enhanced rolling fraction to 48.9%, approaching a similar level to wild-type
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• lymph node T cells from sensitized platelet-treated mutant mice proliferate comparably to wild-type in response to antigen while T cells from untreated sensitized mutants do not proliferate at all
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Find Mice |
Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Selltm1Pest mutation
(0 available);
any
Sell mutation
(41 available)
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immune system
N |
• Selltm1Pest homozygotes show a normal acute response to irritants, including recruitment of nonspecific effector cells such as macrophages and granulocytes
• transfer of wild-type T lymphocytes into Sell-deficient mice restores the ability to respond to a contact hypersensitivity agent
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• spleens of mutants are increased in size by more than 30%
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• mutants show splenic T cell numbers 25% greater than wild-type
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• lymphocyte numbers in mutant nodes are decreased almost 90% but percentages of CD4 and CD8 T cells, and B cells are similar to wild-type mice
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• mice show a dramatic decrease in weights of popliteal lymph nodes (PLNs) compared to wild-type mice
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• mice do not develop antigen-specific T cells in response to a contact hypersensitivity challenge
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• in Sell-deficient mice, antigen-specific T cells are defective in homing to peripheral lymph nodes and subsequent activation in these nodes
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• leukocytes do not exhibit rolling on peripheral node addressin (PNAd), the major ligand for L-Selectin on endothelial venules
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• after skine exposure to DNFB, lymph nodes examined 5 hours later after incubation with DNBS show 97% less T cell proliferation compared to wild-type lymph node T cells
• lymph node T cells proliferate comparably in vitro to wild-type controls in response to polyclonal activation with PMA + Ionomycin, concanavalin A or CD3 antibodies
• when dendritic cells are conjugated with DNBS and injected intravenously or subcutaneously, proliferation of T cells is substantial in splenic T cell cultures but proliferation in lymph node cultures is similar to background; in wild-type mice, T cell proliferation in splenic cultures occurs, but to a lesser extent than in lymph node cultures; results indicate that once response dependence on peripheral lymph nodes is removed, delayed type hypersensitization immune responses are intact
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• antigen applied to epidermis of mutants is taken up by I-A+ dendritic cells which migrate in normal numbers to PLNs but not to other secondary lymphoid tissues
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hematopoietic system
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• in Sell-deficient mice, antigen-specific T cells are defective in homing to peripheral lymph nodes and subsequent activation in these nodes
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• leukocytes do not exhibit rolling on peripheral node addressin (PNAd), the major ligand for L-Selectin on endothelial venules
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• after skine exposure to DNFB, lymph nodes examined 5 hours later after incubation with DNBS show 97% less T cell proliferation compared to wild-type lymph node T cells
• lymph node T cells proliferate comparably in vitro to wild-type controls in response to polyclonal activation with PMA + Ionomycin, concanavalin A or CD3 antibodies
• when dendritic cells are conjugated with DNBS and injected intravenously or subcutaneously, proliferation of T cells is substantial in splenic T cell cultures but proliferation in lymph node cultures is similar to background; in wild-type mice, T cell proliferation in splenic cultures occurs, but to a lesser extent than in lymph node cultures; results indicate that once response dependence on peripheral lymph nodes is removed, delayed type hypersensitization immune responses are intact
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• spleens of mutants are increased in size by more than 30%
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• mutants show splenic T cell numbers 25% greater than wild-type
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cellular
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• in Sell-deficient mice, antigen-specific T cells are defective in homing to peripheral lymph nodes and subsequent activation in these nodes
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• leukocytes do not exhibit rolling on peripheral node addressin (PNAd), the major ligand for L-Selectin on endothelial venules
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• after skine exposure to DNFB, lymph nodes examined 5 hours later after incubation with DNBS show 97% less T cell proliferation compared to wild-type lymph node T cells
• lymph node T cells proliferate comparably in vitro to wild-type controls in response to polyclonal activation with PMA + Ionomycin, concanavalin A or CD3 antibodies
• when dendritic cells are conjugated with DNBS and injected intravenously or subcutaneously, proliferation of T cells is substantial in splenic T cell cultures but proliferation in lymph node cultures is similar to background; in wild-type mice, T cell proliferation in splenic cultures occurs, but to a lesser extent than in lymph node cultures; results indicate that once response dependence on peripheral lymph nodes is removed, delayed type hypersensitization immune responses are intact
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growth/size/body
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• spleens of mutants are increased in size by more than 30%
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Allelic Composition |
Selltm1Pest/Sell+
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Genetic Background |
involves: 129S4/SvJae * C57BL/6 |
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Find Mice |
Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Selltm1Pest mutation
(0 available);
any
Sell mutation
(41 available)
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immune system
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• leukocytes from heterozygotes show ~50% of wild-type levels of rolling along high endothelial venules (HEV)
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• response of sensitized mice to DFNB (contact hypersensitivity) is not significantly different from wild-type mice
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cellular
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• leukocytes from heterozygotes show ~50% of wild-type levels of rolling along high endothelial venules (HEV)
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hematopoietic system
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• leukocytes from heterozygotes show ~50% of wild-type levels of rolling along high endothelial venules (HEV)
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