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1 arkedly increased in the bone marrow (BM) of NZB mice.
2 sociated with the Nba2 predisposing locus in NZB mice.
3  the development of systemic autoimmunity in NZB mice.
4 e development of the autoimmune phenotype in NZB mice.
5 contribution of CD4 and CD8 cell lineages in NZB mice.
6             Malignant B-1 cells derived from NZB mice, a murine model of spontaneous autoimmunity and
7 be casually related to autoimmune disease in NZB mice and its contribution to lupus-like disease in (
8  results identify an unappreciated defect in NZB mice and provide further evidence that generation of
9 g I-Ez or congenic B6 mice carrying H2z with NZB mice and used a backcross analysis to test the hypot
10 otype is also seen in the New Zealand Black (NZB) mice and simultaneously addressed the underlying me
11  CD4 and CD8 gene-deleted New Zealand black (NZB) mice and, as controls, B6.CD4 -/-, B6.CD8 -/-, NZB,
12 ble mice and that SNERV encodes for Sgp3 (in NZB mice) and Gv-1 loci (in 129 mice).
13 ncy in the number of alveolar macrophages in NZB mice appears to be central to enhanced disease, beca
14                           New Zealand Black (NZB) mice are a naturally occurring, late-onset mouse mo
15 lls from autoimmune-prone New Zealand Black (NZB) mice are less efficient at colonizing fetal thymic
16 emolytic anemia (AIHA) in New Zealand Black (NZB) mice, are unknown.
17 the malignant transformation of B-1 cells in NZB mice, backcross animals were studied for the linkage
18             In autoimmune New Zealand Black (NZB) mice, bone marrow small pre-B cells (IgM-CD43-B220+
19 colony forming units (CFU) were also seen in NZB mice by 6 to 8 months of age and accompanied alterat
20 approach was to prevent Band 3 expression in NZB mice by disrupting the AE1 gene.
21 y interfere with B cell development in aging NZB mice by preventing IL-7-mediated proliferation.
22      We have found that resting B cells from NZB mice demonstrate a pronounced defect, compared with
23           Conversely, here we report that in NZB mice, despite the efficient induction of immunoregul
24                             Conplastic (BL/6(NZB) ) mice develop less severe OA compared to the BL/6(
25 memory errors committed over sessions, while NZB mice did not.
26 vels in the spleens of MCMV-infected NZW and NZB mice differed greatly.
27 th melanoma or colon cancer cells, the mtDNA(NZB) mice exhibited strikingly impaired tumor growth whi
28 broader autoimmunity relevance, ICPi-treated NZB mice experienced accelerated onset and severity of l
29                             Autoimmune-prone NZB mice had low endogenous levels of Daf1 irrespective
30 controls, homozygous IFN-alpha/betaR-deleted NZB mice had significantly reduced anti-erythrocyte auto
31  direct observations of T cell precursors in NZB mice have been performed.
32 nations of C57BL/6 (B6; low gp70 levels) and NZB mice (high gp70 levels) to examine the contribution
33                                              NZB mice infected with B. burgdorferi developed higher d
34 monoclonal IgM antibodies derived from older NZB mice inhibit pre-B cell growth to IL-7.
35                  The average onset of CLL in NZB mice is 12 months, but CLL cells can be detected in
36        Rather, the T lymphopoietic defect of NZB mice is due to an impaired ability of pluripotent he
37 e pleiotropic molecules, we created congenic NZB mice lacking the alpha-chain of IFN-alpha/betaR, the
38                               IRF8-deficient NZB mice, lacking pDCs, showed almost complete absence o
39 activity and the response to B. burgdorferi, NZB mice, models of autoimmunity, were infected.
40                    Our data demonstrate that NZB mice produced higher levels of sera IFN-alpha after
41 hereas pDCs from the spleens of NZB/W F1 and NZB mice produced more IFNalpha than pDCs from the splee
42                                     AE1(-/-) NZB mice produced RBC autoantibodies at the same levels
43 ineage precursor cells and IL-7 CFU in vivo, NZB mice produced serum IgM antibodies that strongly inh
44   Splenic T-helper (Th) cells from wild-type NZB mice proliferated strongly against multiple Band 3 p
45   In addition, B cells from autoimmune-prone NZB mice show high levels of RAG messenger RNA and recom
46                           New Zealand Black (NZB) mice spontaneously develop autoimmune disease, usua
47 dependent on the type I IFN receptor even in NZB mice that require type I IFN signaling for spontaneo
48                           The joints of BL/6(NZB) mice that were operated presented more cellularity
49 d a lower apoptosis in the cartilage of BL/6(NZB) mice that were operated.
50 etion does not modify disease progression in NZB mice, thereby strongly implicating IFN-alpha subtype
51 e ability of common lymphoid precursors from NZB mice to repopulate the thymus was not defective.
52 to result in enhanced autoimmune phenotypes, NZB mice were bred with B6 or B6.Sle1c congenic mice and
53                          Although PHSCs from NZB mice were not as efficient at thymic repopulation as
54                                 Alternately, NZB mice were profoundly susceptible to MCMV infection.
55 t mutation in an intron of the Nlrp3 gene in NZB mice, which generates a novel splice acceptor site.
56                          Raltegravir-treated NZB mice, which share the H-2 haplotype with BALB/c mice
57 nd after RSV infection in New Zealand black (NZB) mice, which have constitutive deficiencies in macro
58                           New Zealand black (NZB) mice with autoimmune and B lymphoproliferative dise