Disease relevance of Mice, Inbred NZB

• In contrast, three NZB murine lymphoid cell lines obtained from NZB mice free of hematopoietic neoplasm can grow as well in cystine-deficient media containing L-cystathionine (CSN), the immediate precursor of CYS in the biosynthetic pathway, as in cystine sufficient medium [1].
• Splenic lymphocyte proteins from New Zealand Black (NZB) mice, which spontaneously develop autoimmune disease, and several control strains were analyzed by two-dimensional polyacrylamide gel electrophoresis [2].
• This locus, called Sgp3 (serum gp70 production 3), selectively regulated the production of serum gp70, thereby contributing to the formation of nephritogenic gp70 IC and glomerulonephritis, in combination with Nba2 and Nba5 in NZB mice [3].
• Investigation of biosynthesis of J chain in plasmacytomas induced in NZB mice revealed that this protein was not only synthesized in the cells that produce polymer immunoglobulin A but also in those that produce immunoglobulin G monomer [4].
• The NZB mouse is genetically predisposed to the development of autoimmune disease that resembles the human autoimmune systemic lupus erythematosus and autoimmune hemolytic anemia, with increased titers of anti-DNA, and Coombs' autoantibodies [5].

High impact information on Mice, Inbred NZB

• To directly examine the contribution of these pleiotropic molecules, we created congenic NZB mice lacking the alpha-chain of IFN-alpha/betaR, the common receptor for the multiple IFN-alpha/beta species [6].
• Type-I interferon receptor deficiency reduces lupus-like disease in NZB mice [6].
• This "Ly-1 B" subpopulation (identified and characterized by multiparameter FACS analyses) consists of relatively large, high IgM/low-IgD/low-Ly-1 lymphocytes that represent approximately 2% of the spleen cells in normal animals and, generally, 5-10% of spleen cells in NZB mice [7].
• Studies with FACS-sorted cells show that the presence of Ly-1 on these IgM-secreting cells distinguishes them from the (Ly-1 negative) IgM-secreting "direct" plaque-forming cells generated in NZB mice after stimulation with sheep erythrocytes [7].
• We have found that serum from some (NZB x CBA)F1 mice agglutinated erythrocytes from certain Coombs-positive NZB mice, often in extremely high titer, whereas other (CBA x NZB)F1 sera agglutinated erythrocytes from different individual NZB mice [8].

Biological context of Mice, Inbred NZB

• The CBA/N X chromosome carries a gene, xid, that is associated with the lack of a B cell subset necessary for most of the spontaneous autoantibody production by NZB mice [9].
• IgM serum antibodies and monoclonal IgM antibodies derived from older NZB mice inhibit pre-B cell growth to IL-7 [10].
• Modulation of autoimmunity in NZB mice by cyclophosphamide-induced, nonspecific suppressor cells [11].
• Variations in expression of xenotropic murine leukemia virus genomes in lymphoid tissues of NZB mice [12].
• The present genetic studies using (NZB X NZW)F1 X NZW backcross mice and their second through fourth generation progeny revealed that Agp-1 and Ads-1 exist in common or are closely linked on chromosome 17 of NZB mice and are related to the occurrence of renal disease [13].

Anatomical context of Mice, Inbred NZB

• Expression of NPY mRNA in megakaryocytes in rat bone marrow and NZB mouse spleen was confirmed by in situ hybridization [14].
• Frequencies of 25 immunoglobulin heavy-chain and kappa light-chain variable (VH + V kappa) gene-family pairings expressed in splenic B-cell populations were determined by hybridization of VH- and V kappa-family-specific DNA probes to mitogen-induced B-cell colonies from C57BL/6 mice or hybridomas derived from BALB/c and NZB mice [15].
• Peptides containing a dominant T-cell epitope from red cell band 3 have in vivo immunomodulatory properties in NZB mice with autoimmune hemolytic anemia [16].
• A group of NZB mice received six biweekly injections of cyclophosphamide-induced nonspecific suppressor cells, with treatment commencing at 2 mo of age [11].
• Similarly, B-1 cells from the peritoneal cavity and spleen of autoimmune-prone NZB mice exhibited reduced susceptibility to Fas-mediated apoptosis relative to their B-2 counterparts [17].

Associations of Mice, Inbred NZB with chemical compounds

• NZB mice showed glucose intolerance especially at ages 10 and 30 wk [18].
• This result suggested an androgen insensitivity in NZB mice with regard to NTA production [19].
• The in vivo administration of bacterial lipopolysaccharide to young NZB mice did not stimulate the enlargement of Lyt-2+ T cells [20].
• The higher responses in females and suppression by testosterone were true for all mice studied except NZB mice [21].
• Groups of NZB mice, beginning at 6 mo of age, were fed a vitamin A-deficient diet or a control diet ad libitum or pair-fed to the deficient group [22].

Gene context of Mice, Inbred NZB

• NZB mice that failed to respond to WEHI-3-derived G-CSF also failed to respond to MCGF [23].
• IL-4 and IL-10 modulate autoimmune haemolytic anaemia in NZB mice [24].
• In contrast, NZB mice fail to show significant expression of Ep-CAM even well into adulthood [25].
• The production of such autoantibodies may interfere with B cell development in aging NZB mice by preventing IL-7-mediated proliferation [10].
• To further examine the in vivo requirement for IL-10 in the development and expansion of malignant B-1 clones in NZB mice, we developed a strain of homozygous IL-10 knockout (KO) mice on an NZB background [26].

Analytical, diagnostic and therapeutic context of Mice, Inbred NZB

• An immunofluorescence inhibition assay revealed the presence of autoantibodies with specificities of each NTA260 and NTA204 in the sera from NZB mice [27].

References