Search Criteria: Research Area is "Immunology and Inflammation Research: Immunodeficiency (defects in humoral immune responses)"
| Stock Number |
Strain Name Strain Description |
Standard Supply |
| 000458 | B10.PL-H2u H2-T18a/(73NS)SnJ | Level 3 |
| 000687 | SM/J | Level 4 |
| SM/J mice carry a number of rare polymorphic alleles and are often matched to LG/J (Stock No. 000675), A/J (Stock No. 000646) or NZB/BINJ (Stock No. 000684) for quantitative trait locus analysis. These mice are susceptible to diet-induced obesity and diet-induced atherosclerosis. SM/J mice exhibit a hyperresponsiveness to B cell mitogens (Clark et al. 1981, Engel et al. 1981). A point mutation in Neu1 is responsible for a partial deficiency of lysosomal neuraminadase and may explain the altered immune response (Rottier et al. 1998). Small in size at birth and through weaning, SM/J mice attain a normal body weight as they age. | ||
| 006353 | B6.129-Btlatm1Kmm/J | Repository- Live |
| Mice that are homozygous for the targeted mutation are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. No gene product (mRNA) is detected by Northern blot analysis of splenocytes isolated from homozygous animals. Mutant mice exhibit increased sensitivity to antigen-induced experimental autoimmune encephalomyelitis (EAE), a mouse model of multiple sclerosis). T-cell proliferation is enhanced in response to antigen challenge. Although acute experimental allergic airway inflammation intensity is only slightly increased, the response duration is significantly prolonged. This mutant mouse strain may be useful in studies of immune response and autoimmunity, and in transplantation studies.
In an attempt to offer alleles on well-characterized or multiple genetic backgrounds, alleles are frequently moved to a genetic background different from that on which an allele was first characterized. It should be noted that the phenotype could var
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| 006621 | B6.129P2(C)-Ccr7tm1Rfor/J | Repository- Live |
| Homozygous mice are viable and fertile and show delayed primary B or T cell immune responses. Lymph nodes from homozygous mice are devoid of naive T cells and dendritic cells (DCs), but the T cell populations in the blood, the red pulp of the spleen, and in the bone marrow are greatly expanded. Secondary lymph organs exhibit morphological abnormalities, and adoptive transfer experiments demonstrate impaired B- and T-cell migration. In a model of acute allogeneic tumor rejection, homozygous mice fail to reject subcutaneously injected MHC class I mismatched tumor cells, and cytotoxic activity of allospecific T cells is severely compromised. These mutant mice (along with CXCR5-deficient mice - Stock No. 006659) - may be useful in immunological studies of chemokine receptors, including T- and B-cell function in primary and adaptive immune responses, entry of lymphocytes and dendritic cells into secondary lymphoid organs (and their hom
..... For more information please see the full descriiption on the strain data sheet | ||
| 006301 | B6.129S-Id3tm1Zhu/J | Repository- Live |
| Mice that are homozygous for the targeted mutation are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. No gene product (mRNA) is detected by Northern blot analysis from spleen tissue. Homozygotes exhibit reduced basal IgG1 and IgG2a levels. When challenged with keyhole limpet hemocyanin coupled to DNP, production of IgG2a and IgG3 was 10% and 6% of the wildtype response after primary and secondary challenges, respectively. DNP-Ficoll challenge results in a 90% reduction of IgM and IgA production. Cultured B-cells have diminished proliferation in response to surface IgM stimulation. Keratoconjunctivitis sicca (dry eyes) occurs in 10% of homozygotes aged 6 to 10 months, and in 80% of mice more than 1 year in age. Tear and saliva flow volume is reduced. Histological analysis reveals lymphocyte infiltration and tissue degradation in lachrymal and salivary glands. Mutants older than 1 year in age produce autoantibodies, anti-SSA and anti-SS
..... For more information please see the full descriiption on the strain data sheet | ||
| 005763 | B6.129S1-Nod2tm1Flv/J | Repository- Live |
| Homozygous mice are viable and fertile with normal lymphoid and myeloid cellularity and no intestinal inflammation up to 6 months of age. Homozygotes do not express the targeted gene in spleen or intestinal crypts. Null mice, as well as antigen presenting cells derived from them, lack the protective immunity (IgG1, interleukin-6, and NF-kappaB-related responses) normally afforded by endogenous protein recognition of its ligand, bacterial muramyl dipeptide (MDP). Mice homozygous for the mutation have increased susceptibility to oral (intragastric) bacterial challenge and diminished cryptdins. This mouse may be useful in studies of Crohn's disease and other inflammatory bowel diseases, innate immunity, signal transduction, and bacterial susceptibility. | ||
| 006659 | B6.129S2(Cg)-Cxcr5tm1Lipp/J | Repository- Live |
| Homozygous (CXCR5-deficient) mice are viable and fertile. Multiple lymphoid organs lack detectable levels of targeted protein expression using flow cytometry, and RNA transcripts are also absent in spleen cells. Homozygous mutant mice exhibit a complex pattern of lymph node (LN) developmental defects (e.g. deficient in inguinal, iliac and parathymic LN, but apparently normal mesenteric LN) accompanied by impaired Peyer's patch development. In addition, CXCR5-deficient mice show a completely disorganized splenic microarchitecture, lacking segregated T- and B-cell areas within the splenic white pulp. These mutant mice (along with CCR7-deficient mice: Stock No. 006621) may be useful in immunological studies of chemokine receptors, including T- and B-cell function in primary and adaptive immune responses, entry of lymphocytes and dendritic cells into secondary lymphoid organs and their homing to T- and B-cell zones therein.
In
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| 006198 | B6.129S4-Matktm1Sor/J | Repository- Live |
| Homozygotes are viable and fertile with no behavioral abnormalities. The donating investigator reports homozygous mutants have no endogenous protein expression. Homozygous mice have an approximately 2-fold increase in the primitive hematopoietic stem cell population SPKLS (c-Kit+, Lin-, Sca-1+ in combination with side population cells). Homozygous deficiency also leads to the hyperproliferation of pre-B cells in the presence of Interleukin-7, and impaired IFN-gamma production in lymph and spleen cells upon in vivo antigen challenge. These mutant mice may be useful in studying tyrosine phosphorylation of hematopoietic cells, primitive/early hematopoietic populations, immune cell signaling, and regulation of immunological responses. | ||
| 006122 | B6.129S4-Mbl1tm1Kata Mbl2tm1Kata/J | Repository- Live |
| Mice homozygous for both mannose-binding lectin (MBL)-A and MBL-C targeted mutations (termed MBL-null) are viable, fertile, and normal in size with no obvious developmental defects. Histological examination of multiple organs from 6-10 week old mice shows no abnormalities. MBL-null mice have no endogenous gene expression in liver (the principal site of MBL synthesis) and no protein detectable in serum. While the classical complement pathway is unaffected in MBL-null mice, the lectin-dependent complement pathway is non-functional. MBL-null mice have increased mortality following intravenous injection of S. aureus associated with abnormal serum levels of TNFalpha and IL-6 (decreased at 2h, elevated at 24h post injection). Cyclophosphamide-induced febrile neutropenic MBL-null mice inoculated with S. aureus have greatly increased susceptibility to abscess formation in kidney, liver, and lung (but not spleen). These same treated mice also have persistent bacteremia despite a r
..... For more information please see the full descriiption on the strain data sheet | ||
| 006259 | B6.Cg-Pepcb Ptprca Tg(UBC-scFv)2Nemz/J | Repository- Live |
| "Kappa-macroself Ag#2" transgenic mice express a membrane-bound "macroself" superantigen with specificity for the mouse immunoglobulin kappa light chain (IgΚ). Hemizygous mice are viable and fertile. The transgene is expressed in virtually all cells tested, including lymphoid tissue and bone marrow. B cells expressing the IgΚ-macroself superantigen are absent from the peripheral lymphoid organs while Igl+ B cell numbers are substantially increased. Although bone marrow B cell numbers are unchanged, total peripheral B cell populations are reduced by approximately one half. These mice also express the CD45.1 (Ly5.1 or Ptprca) allele, which is atypical for this C57BL/6 (B6) congenic background, and this marker may be used to track donor cell populations in bone marrow transplantation studies with B6 (CD45.2: Ptprcb) mice.
These "kappa-macroself Ag#2" transgenic mice may be useful to study B cell receptor editing and B cell tolerance in a polyclona
..... For more information please see the full descriiption on the strain data sheet | ||
| 003127 | FVB;129P2-Bcl3tm1Ver/J | Repository- Live |
| Mice homozygous for the Bcl3 targeted mutation are viable and fertile and display no alterations in their behavior or gross anatomy. While normal numbers of both T and B cell lymphocytes are produced, homozygous mutants display severe defects in humoral immune responses. Normal immunoglobulin levels are observed, but the mice are unable to clear Listeria monocytogenes or Streptococcus pneumoniae, thus indicating the necessity of Bcl3 in the production of antigen-specific antibodies. Additionally, splenic white pulp is devoid of germinal centers in the homozygous null mice. | ||
| 006355 | NOD.129-Btlatm1Kmm/J | Repository- Live |
| Mice that are homozygous for the targeted mutation are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. No gene product (mRNA) is detected by Northern blot analysis of splenocytes isolated from homozygous animals. Mutant mice exhibit increased sensitivity to antigen-induced experimental autoimmune encephalomyelitis (EAE), a mouse model of multiple sclerosis). T-cell proliferation is enhanced in response to antigen challenge. Although acute experimental allergic airway inflammation intensity is only slightly increased, the response duration is significantly prolonged. This mutant mouse strain may be useful in studies of immune response and autoimmunity, and in transplantation studies.
In an attempt to offer alleles on well-characterized or multiple genetic backgrounds, alleles are frequently moved to a genetic background different from that on which an allele was first characterized. It should be noted that the phenotype could var
..... | ||
| 006339 | C.129-Btlatm1Kmm/J | Repository-Cryopreserved |
| Mice that are homozygous for the targeted mutation are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. No gene product (mRNA) is detected by Northern blot analysis of splenocytes isolated from homozygous animals. Mutant mice exhibit increased sensitivity to antigen-induced experimental autoimmune encephalomyelitis (EAE), a mouse model of multiple sclerosis. T-cell proliferation is enhanced in response to antigen challenge. Although acute experimental allergic airway inflammation intensity is only slightly increased, the response duration is significantly prolonged. This mutant mouse strain may be useful in studies of immune response and autoimmunity, and in transplantation studies.
In an attempt to offer alleles on well-characterized or multiple genetic backgrounds, alleles are frequently moved to a genetic background different from that on which an allele was first characterized. It should be noted that the phenotype could vary
..... | ||
| 006052 | STOCK Ighg1tm1.1Ksho/J | Repository-Cryopreserved |
| Mice homozygous for the targeted allele are viable and fertile. Both heterozygous and homozygous mutants demonstrate impaired primary and secondary IgG1 responses. Serum IgG1 concentrations in homozygous mutant mice are reduced 71-fold compared to controls. This mutant mouse strain may be useful in studies of the role of IgG1 immunoglobulins in immune responses and in the generation of plasma cells and memory B cells. | ||
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