ライフサイエンスコーパス: NZB mice

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 ncy in the number of alveolar macrophages in NZB mice appears to be central to enhanced disease, beca

13 New Zealand Black (NZB) mice are a naturally occurring, late-onset mouse mo

14 lls from autoimmune-prone New Zealand Black (NZB) mice are less efficient at colonizing fetal thymic

15 emolytic anemia (AIHA) in New Zealand Black (NZB) mice, are unknown.

16 the malignant transformation of B-1 cells in NZB mice, backcross animals were studied for the linkage

17 In autoimmune New Zealand Black (NZB) mice, bone marrow small pre-B cells (IgM-CD43-B220+

18 colony forming units (CFU) were also seen in NZB mice by 6 to 8 months of age and accompanied alterat

19 approach was to prevent Band 3 expression in NZB mice by disrupting the AE1 gene.

20 y interfere with B cell development in aging NZB mice by preventing IL-7-mediated proliferation.

21 We have found that resting B cells from NZB mice demonstrate a pronounced defect, compared with

22 Conversely, here we report that in NZB mice, despite the efficient induction of immunoregul

23 memory errors committed over sessions, while NZB mice did not.

24 vels in the spleens of MCMV-infected NZW and NZB mice differed greatly.

25 Autoimmune-prone NZB mice had low endogenous levels of Daf1 irrespective

26 controls, homozygous IFN-alpha/betaR-deleted NZB mice had significantly reduced anti-erythrocyte auto

27 direct observations of T cell precursors in NZB mice have been performed.

28 nations of C57BL/6 (B6; low gp70 levels) and NZB mice (high gp70 levels) to examine the contribution

29 NZB mice infected with B. burgdorferi developed higher d

30 monoclonal IgM antibodies derived from older NZB mice inhibit pre-B cell growth to IL-7.

31 The average onset of CLL in NZB mice is 12 months, but CLL cells can be detected in

32 Rather, the T lymphopoietic defect of NZB mice is due to an impaired ability of pluripotent he

33 e pleiotropic molecules, we created congenic NZB mice lacking the alpha-chain of IFN-alpha/betaR, the

34 IRF8-deficient NZB mice, lacking pDCs, showed almost complete absence o

35 activity and the response to B. burgdorferi, NZB mice, models of autoimmunity, were infected.

36 Our data demonstrate that NZB mice produced higher levels of sera IFN-alpha after

37 hereas pDCs from the spleens of NZB/W F1 and NZB mice produced more IFNalpha than pDCs from the splee

38 AE1(-/-) NZB mice produced RBC autoantibodies at the same levels

39 ineage precursor cells and IL-7 CFU in vivo, NZB mice produced serum IgM antibodies that strongly inh

40 Splenic T-helper (Th) cells from wild-type NZB mice proliferated strongly against multiple Band 3 p

41 In addition, B cells from autoimmune-prone NZB mice show high levels of RAG messenger RNA and recom

42 New Zealand Black (NZB) mice spontaneously develop autoimmune disease, usua

43 dependent on the type I IFN receptor even in NZB mice that require type I IFN signaling for spontaneo

44 etion does not modify disease progression in NZB mice, thereby strongly implicating IFN-alpha subtype

45 e ability of common lymphoid precursors from NZB mice to repopulate the thymus was not defective.

46 to result in enhanced autoimmune phenotypes, NZB mice were bred with B6 or B6.Sle1c congenic mice and

47 Although PHSCs from NZB mice were not as efficient at thymic repopulation as

48 Alternately, NZB mice were profoundly susceptible to MCMV infection.

49 t mutation in an intron of the Nlrp3 gene in NZB mice, which generates a novel splice acceptor site.

50 Raltegravir-treated NZB mice, which share the H-2 haplotype with BALB/c mice

51 nd after RSV infection in New Zealand black (NZB) mice, which have constitutive deficiencies in macro

52 New Zealand black (NZB) mice with autoimmune and B lymphoproliferative dise