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1 ransplantation method, into old or young Ly5 congenic mice.
2 severe EAE in NOD mice compared with Idd5.1 congenic mice.
3 mechanism of protection from diabetes in Idd congenic mice.
4 notype of the lupus-like disease in NZM 2328 congenic mice.
5 14- to 15-day fetal thymic lobes from Thy-1 congenic mice.
6 The locus on chromosome 2 was confirmed in congenic mice.
7 P-1 were evaluated for immunogenicity in B10 congenic mice.
8 n and injected into lethally irradiated Ly-5 congenic mice.
9 mice showed responses similar to the normal congenic mice.
10 cra(b) with Tcra(a) or Tcra(c) haplotypes in congenic mice.
11 c segment of CD45 were transferred into CD45 congenic mice.
12 e in hypersusceptible BALB/c.DBA/2-Idh1-Pep3 congenic mice.
13 + expansion was absent in H-2IA(b)-deficient congenic mice.
14 transgenic cells adoptively transferred into congenic mice.
15 leads to autoimmune cholangitis in NOD.Abd3 congenic mice.
16 on intratracheal adoptive cell transfer into congenic mice.
17 g the systemic administered MDSC from CD45.1 congenic mice.
18 f them had fat mass as large as the original congenic mice.
19 controls, and comparable that to B6.TH-tabw2 congenic mice.
20 optively transferred into Rag1((-)/(-))Ly5.1 congenic mice.
21 ne marrow-derived dendritic cells from Cdcs1 congenic mice.
22 e measured in aging female gld and wild-type congenic mice.
23 s following the transfer of these cells into congenic mice.
24 gher resolution than that attained using the congenic mice.
25 ress the IgM(b) allotype) to IgM(a) allotype congenic mice.
26 lymphoid and myeloid progenitors from CD45.1 congenic mice.
27 fertile but weighed significantly less than congenic +/+ mice.
30 ypes, NZB mice were bred with B6 or B6.Sle1c congenic mice and approximately 20 female offspring were
31 were compared between cohorts of B6.Sle2.lpr congenic mice and B6.lpr mice of ages up to 6 months.
34 LB/c mice with NK cells from BALB.B6-Cmv1(r) congenic mice and generated a mAb, designated 4E4, that
35 gene mRNA expression data in segregating and congenic mice and identify glutamate receptor metabotrop
37 We confirmed the presence of Blmpf1 in MHC congenic mice and narrowed the region to 2.7 cM in a red
38 QTL was coincident with a body weight QTL in congenic mice and Scg5 expression was negatively correla
40 9S-Cdh23(c.753A) SNV and 129S1.B6-Cdh23(ahl) congenic mice, and a linkage backcross involving these s
41 ast, spontaneous virus-expressing AKR.H-2(b) congenic mice are low/nonresponders for the generation o
44 to nearly those of wild-type B6 in the B6/B6 congenic mice as follows: 83% rescue of low pial collate
47 blockade but is prolonged further in NOD Idd congenic mice bearing C57-derived chromosome 3 loci.
49 eous proliferation when transferred to naive congenic mice, both characteristic of central memory T c
50 not in C3H/HeJ or BALB/c (C.C3H Tlr4(lps-d)) congenic mice, both of which have a mutant TLR4 gene.
51 e or absence of the Stat5b mutation in these congenic mice but is correlated with the expression leve
54 chimerism was studied in nonirradiated Ly 5 congenic mice by quantitative intrathymic and intravenou
55 tandard backcross breeding scheme to produce congenic mice by the inclusion of genotype-based selecti
56 he profound protection from diabetes seen in congenic mice carrying an Idd3 protective allele is unli
63 used NZB.NZW-Lbw2 congenic (designated Lbw2 congenic) mice containing an introgressed fragment of Ne
64 + CD25- cells transferred into thymectomized congenic mice converted to CD4+ CD25+ cells that also su
66 ive transplant model, which uses Ly5.2/Ly5.1 congenic mice, cytokine-cultured Ly5.2 cells competed wi
67 gh-resolution marker of neuronal activation, congenic mice demonstrated significantly less neuronal a
68 on and IL-17 production in interval-specific congenic mice demonstrated that the two identified genet
69 rom T1D to the same extent as NOD.B10 Idd5.1-congenic mice, demonstrating that increased liCTLA-4 exp
76 oliferator-activated receptor-gamma, and the congenic mice exhibited significantly reduced expression
77 ogenitor responded equally to DMBA and BP in congenic mice expressing the PAH-resistant AhR (AhR(d)).
78 generating lines of transgenic B10 (H-2(b)) congenic mice expressing three independent contiguous co
79 ich Nba2 genes accomplish this, we generated congenic mice expressing various Nba2 intervals where ge
80 ficantly dysregulated in arthritic joints of congenic mice; expression of these genes was also sex sp
81 Lyme arthritis in the reduced interval Bbaa1 congenic mice, formally implicating myostatin as a novel
84 t alcohol-avoiding male B6.D2 Alcp1 line 2.2 congenic mice have lower Ucn immunoreactivity in the EW
86 s (Tregs), and we found that B10.S-Eae5(SJL) congenic mice have significantly greater numbers of lymp
87 ice with that observed in diabetes-resistant congenic mice having protective alleles at insulin-depen
89 MHV-68-specific CD4(+) T cells generated in congenic mice homozygous for disruption of the beta2-mic
90 chromosome 2 that could not be confirmed in congenic mice, however, probably because of epistasis.
92 Bone marrow-derived macrophages from Bbaa1 congenic mice implicated this locus as a regulator of ty
93 by comparing alpha7 receptor development in congenic mice in which the DBA/2 allele of Chrna7 has be
94 welve-month-old C3H.SW-H2b/SnJ mice (C3H/HeJ congenic mice in which the H2k purported susceptibility
95 diation sensitivity, we conducted studies on congenic mice in which the linked region on chromosome 1
96 trains (often C57BL/6J) typically results in congenic mice in which the targeted gene is flanked by E
98 ordance of phenotypes between Tgfb2(+/-) and congenic mice indicates that HSPC frequency and cycling
103 ated effector CD4(+) T cells into tumor-free congenic mice mediates rejection of tumor challenge 9 mo
105 total) to detect underlying genetic loci; 2) congenic mice (n = 23) to replicate the identified locus
106 1 diabetes, and changes between NOD and NOD congenic mice (NOD.Idd3/Idd10 and NOD.B10Sn-H2(b)), whic
108 round or DR4.Ab(0)- and DQ8.Ab(0)-transgenic/congenic mice on the arthritis-susceptible BALB/c geneti
109 dependency, we used genetically modified and congenic mice on the C57BL/10 background and in vitro T-
110 hat macrophages obtained from sst1-resistant congenic mice possess superior ability to kill L. monocy
112 m multilineage chimerism is achieved in CD45 congenic mice receiving high bone marrow doses with or w
113 tion of these cells into lethally irradiated congenic mice resulted in efficient gene transfer into h
114 using major histocompatibility complex (MHC)-congenic mice revealed probable contributions by both MH
115 ysis of iNKT cell number and function in Idd congenic mice revealed that neither iNKT cell number nor
116 Transplantation of Vk*MYC tumor cells into congenic mice selected for a more aggressive disease tha
117 ained with independent inbred strains and H2 congenic mice show that the genetic control of all three
122 ted at human chromosome 5q23-35, we examined congenic mice that differed at the homologous chromosoma
123 have developed novel NOD.B10-Idd9 (line 905) congenic mice that predominantly harbor islet-reactive C
124 tations to the reported genetically modified congenic mice that were generated using 129-strain ESCs
130 s can be fine-mapped by crossing appropriate congenic mice to the background strain, and complex gene
131 ting the cells into lethally irradiated Ly-5 congenic mice together with "compromised" marrow cells.
132 ransplantation into lethally irradiated Ly-5 congenic mice together with compromised marrow cells.
133 e cultured cells to lethally irradiated Ly-5 congenic mice together with compromised marrow cells.
134 These results validate the approach of using congenic mice together with genome-wide analysis of tiss
135 esis of EAE, we generated phenotype-selected congenic mice using EAE-resistant B10.S and EAE-suscepti
136 In our present study, we generated Par1 congenic mice using two mouse strains A/J (Par1/-) and M
138 d that increased expression of Ifi202 in the congenic mice was associated with inhibition of E2F1-med
141 strain mapping using autoimmune NOD.C57BL/6J congenic mice, we demonstrated previously that the type
144 ransfer of CD45.1-positive cells into CD45.2 congenic mice, we show that CD11c(+)Gr-1(+) cells migrat
149 ient (C5(-/-)) macrophages derived from B.10 congenic mice were found to be defective in killing intr
150 erived LSK(-) cells upon transfer into naive congenic mice were found to differentiate predominantly
151 type C57/Bl6 mice and LDL-receptor deficient congenic mice were randomly assigned for infection with
152 After colonic preparation, 20 anesthetized congenic mice were scanned with high-resolution microCT.
153 in-dependent variation as well, we generated congenic mice where the telomeric region of chr.4 was in
154 pared with CD4(+) T cells from NOD.H2(b) MHC-congenic mice (which have an H2(b) MHC region introgress
155 tablished in NOD.Cg-Rag1(tm1Mom)Prf1(tm1Sdz) congenic mice, which are devoid of NK cell activity.
156 In this study, we used C57BL/6.S (B6.S) congenic mice, which carry H-2(s) MHC genes instead of H
157 nificantly increased in the B6.C3H(Dyscalc1) congenic mice, which carry only the Dyscalc1 locus with
158 neration compared with T cells from NOD.Idd3 congenic mice, which carry the protective Idd3 allele fr
159 es in splenic cells from lupus-prone B6.Nba2 congenic mice, which express increased levels of p202, w
160 ing pancreatic IL-10 backcrossed to B10.H2g7 congenic mice, which have no Idd alleles other than NOD
161 hem susceptible to Salmonella, and BALB/c.D2 congenic mice, which have the wild-type Nramp1 gene that
162 ses of CD4(+) T cells from NOD and B6.G7 MHC congenic mice, which share the H2(g7) MHC region but dif
163 that differ genetically only at the MHC (MHC congenic mice), while they cannot distinguish geneticall
164 class II-deficient mice engrafted readily in congenic mice, while HSC from class I-deficient donors (
165 ssion for RP1 disease, the authors generated congenic mice with a gene-targeted retinitis pigmentosa
169 lated from the paws of male and female Pgia8-congenic mice with collagen antibody-induced arthritis.
173 newly identified plasmacytomas from NFS.V(+) congenic mice with plasmacytomas of IL6 transgenic, Fasl
174 these modifier(s), we generated recombinant congenic mice with quantitative trait loci (QTL) contain
175 then compared the phenotypes of these triple congenic mice with that of previously characterized B6.S
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