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1 etic or nonhematopoietic cells, we generated bone marrow chimeras.
2 tion of Ag-specific IMP CD8(+) T cells using bone marrow chimeras.
3 egress was demonstrated by generating mixed bone marrow chimeras.
4 an anti-tumor effect induced by RLI in mixed bone marrow chimeras.
5 stitute the Treg population in the thymus of bone marrow chimeras.
6 g excretion compared with infected wild-type bone marrow chimeras.
7 and on circulating CD8 T cells in the mixed bone marrow chimeras.
8 hemokine Grobeta was abrogated in CXCR4(-/-) bone marrow chimeras.
9 PLZF(-/-) mice and mixed wild-type:PLZF(-/-) bone marrow chimeras.
10 rant of MHC class I-deficient cells in mixed bone marrow chimeras.
11 orylation and reduced platelet production in bone marrow chimeras.
12 sponses of flagellin-treated MyD88 radiation bone marrow chimeras.
13 of CD83-cKO B cells in GC responses in mixed bone marrow chimeras.
14 ls and intrinsic renal cells, we constructed bone marrow chimeras.
15 leting peripheral CD4 T cells or by creating bone marrow chimeras.
16 elium from that of hemopoietic APCs by using bone marrow chimeras.
17 we performed fate-tracing experiments using bone marrow chimeras.
18 ted HO-2(-/-) and wild-type (WT) mice and in bone marrow chimeras.
19 nd this relationship is recapitulated in the bone marrow chimeras.
20 In comparison with BAFF- or APRIL-sufficient bone marrow chimeras, absence of hematopoietic compartme
22 same observation in PHD2(+/+) --> PHD2(+/-) bone marrow chimeras also suggests organization of a bet
23 ce showed a reduced CHS response to DNFB, in bone marrow chimera and adoptive transfer experiments, w
24 ion after DSS-induced injury, as revealed by bone marrow chimera and dendritic cell-depletion experim
25 models and monocytopenic mice, together with bone marrow chimera and parabiotic models, we found that
26 mune responses to HSV-1 were dissected using bone marrow chimeras and adoptive cell transfer approach
31 identify the relevant APC in K14 mice using bone marrow chimeras and found that radioresistant cells
33 function, and we confirmed that result with bone marrow chimeras and in vitro, where the absence of
34 c role in type 2 responses was explored with bone marrow chimeras and induction of gastrointestinal t
38 CD8(+) T-cell response to the VP2 peptide in bone marrow chimeras and mutant mice lacking peripheral
39 rin(+) cells in vivo, together with congenic bone marrow chimeras and parabiotic mice as tools to dif
40 iNKT thymic development in limited-dilution bone marrow chimeras and show that higher TCR avidity co
42 nduces a host-versus-graft reaction in mixed bone marrow chimeras and that rejection of donor cells l
43 CNS during EAE development, we created CD24 bone marrow chimeras and transgenic mice in which CD24 e
44 mice was shown to be B cell intrinsic using bone marrow chimeras and was not due to a developmental
45 s, HLA-DR4-transgenic mice, MAIThighHLA-DR4+ bone marrow chimeras, and humanized NOD-scid IL-2Rgamman
46 13 inbred mouse strains, F1 and F2 hybrids, bone marrow chimeras, and neutrophil function assays.
47 h the use of adoptively transferred T-cells, bone marrow chimeras, and reconstituted severe combined
51 , we used adoptive transfer, transgenic, and bone marrow chimera approaches to show increased infiltr
52 dependent conditional Blimp-1 knockout mixed bone marrow chimera as well as an adoptive transfer appr
53 ed wild-type (wt)-->MHCI-/- or wt-->MHCII-/- bone marrow chimeras as recipients in GVHD experiments.
54 e Foxp3(-) precursors using studies of mixed bone marrow chimeras as well as TCR-specific generation
59 levant accessory cells in vivo, we generated bone marrow chimeras between either wild-type (WT) and M
61 T regulatory cells (Tregs), we studied mixed bone marrow chimeras between wild-type and IFN-alpha/bet
63 role of TLR4 in lung protection, using used bone marrow chimeras; cell-specific transgenic modeling;
67 o failed to inhibit EAE in reciprocal, mixed bone marrow chimeras constructed by transferring IL-10-d
68 beta T cells are poorly established in mixed bone marrow chimeras, contrasting with strong gammadelta
71 VitD receptor-deficient (vdr(-/-)) radiation bone marrow chimeras demonstrate that reductions in pulm
92 Lrrc8a(-/-) mice and Lrrc8a(-/-)-->Rag2(-/-) bone marrow chimeras exhibited a severe cell-intrinsic b
121 prevent autoreactive T cells from deletion; bone marrow chimera experiments suggest that CD24 on rad
132 ressing core protein throughout the body and bone marrow chimeras expressing core protein in either t
135 in LPL-deficient hematopoietic cells, using bone marrow chimeras, failed to rescue the phenotype of
138 Rag2(-/-), but not WT-->IkappaBalpha mutant, bone marrow chimeras formed proper lymphoid organs and d
139 in naive CD8(+) T cells in vivo by creating bone marrow chimera from hematopoietic progenitors trans
140 s to trans present IL-15, we generated mixed bone marrow chimera from IL-15Ralpha- and IL-2/15Rbeta-d
142 ied using reciprocal hematopoietic radiation bone marrow chimeras generated between male wild-type an
145 mal alpha7nAChRs, as shown by experiments in bone marrow chimeras generated with wild-type and alpha7
147 Sepsis induction in C5aR(+)/C5aR(-) mixed bone marrow chimeras identified cognate engagement of C5
152 e T-B interactions, we constructed radiation bone marrow chimeras in which CD4+ T cells would be acti
153 the development of PGIA, we generated mixed bone marrow chimeras in which CD80/CD86 is specifically
154 addressed through analyses of NOD background bone marrow chimeras in which H2(nb1) molecules were sel
155 ized in the transgenic mice and in radiation bone marrow chimeras in which ligand-bearing mice served
156 ing wild-type and DNMAML T cells together in bone marrow chimeras increased accumulation of Notch-dep
158 ransgenic CD4 T cells and studies with mixed bone marrow chimeras indicated that indirect effects and
162 ellular MZ microenvironment, and analysis of bone marrow chimeras indicated that the MZ B cell develo
163 LTbeta(-/-), LTalpha(+/-)beta(+/-) mice and bone marrow chimeras, indicated that rapid protective Th
170 tion of CD4(+) T cell adoptive transfers and bone marrow chimera mice in which the presence or absenc
171 autoimmune encephalomyelitis (EAE), we used bone marrow chimera mice that allowed us to distinguish
172 e macrophage inflammatory phenotype by using bone marrow chimera mice with conditional PU.1 knockout.
173 g the use of p47(phox-/-) mice, p47(phox-/-) bone marrow chimera mice, adoptive transfer of macrophag
180 ze of a differentiating Treg population in a bone marrow chimera model, which correlated with reduced
187 Once niche effects are neutralized in mixed bone marrow chimeras, positive and negative selection ar
191 s transferred into wild-type mice, but mixed bone marrow chimeras receiving wild-type and Crel(-/-)Nf
193 examined this possibility using XX versus XY bone marrow chimeras reconstituted with a common immune
195 in neutrophil trafficking using mouse mixed bone marrow chimeras reconstituted with Cxcr2(-/-) and W
196 was abrogated in IL-4R-deficient mice and in bone marrow chimeras reconstituted with myeloid cells th
199 Adoptive transfer experiments and radiation bone marrow chimera reveal that a Txb21(+/+) environment
201 .L2 WT and n3.L2 PKCtheta(-/-) thymocytes in bone marrow chimeras revealed a more dramatic defect, wi
232 nflammatory responses, and lipid uptake, and bone marrow chimeras suggest that hematopoietic EphA2 de
233 tion of Ly6-G(+) cells and use of C5aR1(-/-) bone marrow chimeras suggested an essential role of C5aR
234 sing from bone marrow precursors in neonatal bone marrow chimeras suggested that Foxp3(+) DP cells ar
235 e with wild-type T cell progenitors in mixed bone marrow chimeras, suggesting that in normal mice, th
236 ed iNKT cell frequencies in Myb heterozygous bone marrow chimeras suggests that miR-150 differentiall
238 rim24 deficiency to T cells by using a mixed bone marrow chimera system and found that T-cell-intrins
239 kely to contribute to disease, we utilized a bone marrow chimera system to distinguish between these
240 using IFN-gamma receptor knockout mice in a bone marrow chimera system, we show that the IFN-gamma p
241 ow-density lipoprotein-deficient (Ldlr(-/-)) bone marrow chimeras that express a transgene containing
242 ment of systemic autoimmune disease by using bone marrow chimeras that lacked expression of major his
247 viduals and, more importantly, use radiation bone marrow chimeras to demonstrate that restriction of
248 ing sepsis, we used CXCL1-deficient mice and bone marrow chimeras to demonstrate the importance of th
251 use mixed G-CSF receptor (G-CSFR)-deficient bone marrow chimeras to show that G-CSF-induced mobiliza
254 n murine T cell function, we generated mixed bone marrow chimeras using bone marrow from NIK knockout
255 ulation in the intestines of Arg I-deficient bone marrow chimeras was associated with intestinal hemo
258 phosphate (NADPH) oxidase 2 (NOX2) and their bone marrow chimera, we demonstrated that NOX2 from both
261 Using reaggregated thymic organ culture and bone marrow chimeras, we demonstrate that positive selec
263 al microscopy with DREAM-null mice and their bone marrow chimeras, we demonstrated that both hematopo
267 horiomeningitis virus-mediated hepatitis and bone marrow chimeras, we found that Bim has a dual role
268 forms of the serine/threonine kinase AKT and bone marrow chimeras, we found that hematopoietic cell-a
269 , PLZF reporter/fate mapping mice, and mixed bone marrow chimeras, we identified two distinct populat
272 receptor (TCR)-transgenic T cells and mixed bone marrow chimeras, we show that activation of naive p
273 udy, using adoptive transfer experiments and bone marrow chimeras, we show that at least some of thes
276 sing reciprocal adoptive transfer models and bone marrow chimeras, we show that Myd88(-/-) CD8 T cell
282 esident cells contribute to ischemic injury, bone marrow chimeras were generated by transplanting bon
286 in T cells under noncompetitive conditions, bone marrow chimeras were generated, in which the T cell
292 F(-/-) mice, wild-type littermates, or mixed bone marrow chimeras were treated with the protease alle
293 ss accumulation in the inflamed CNS in mixed bone marrow chimeras, when compared with CCR2(+/+) DCs;
294 ock-in mice as well as Sap(R78A) competitive bone marrow chimeras, which retained NKT cells but at si
295 lls (TECs) in Treg selection, we constructed bone marrow chimeras with disrupted CD28/B7 signaling in
296 To clarify the latter, we generated murine bone marrow chimeras with enforced Erg expression in eng
298 endothelium-specific deficiency in JAM-A and bone marrow chimeras with JAM-A-deficient leukocytes.
299 Using IL-15(WT/WT) and IL-15(-/-) mice, bone marrow chimeras with normal cellularity, and a sele
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