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1                                         Both scurfy and normal T cells are responsive to two distinct
2 CD4+ T cells enabled the long-term rescue of scurfy autoimmune disease.
3 T cell proliferation in vitro and rescue the scurfy autoimmune phenotype in vivo.
4                                  Transfer of Scurfy CD4(+) T cells into nu/nu mice yielded autoantibo
5 at the adoptive transfer of FOXP3-transduced scurfy CD4+ T cells enabled the long-term rescue of scur
6 a T cells in the TCRalpha(-/-) recipients of scurfy cells markedly expanded and expressed a highly ac
7 provided by the TCR and by ligation of CD28; scurfy cells, however, are hyperresponsive to TCR ligati
8     Furthermore, complementation of Foxp3 in scurfy-derived T cells lowers the NFAT and NF-kappa B tr
9 odel highlighted the possibility of rescuing scurfy disease after the latter's onset.
10              In addition, development of the Scurfy disease also may require mutation of the gene in
11 reproduces the inflammatory phenotype of the scurfy donor, including hepatitis and pneumonitis.
12 tute immunodeficient mice in the presence of scurfy fetal liver cells.
13                       In mixed chimeras with Scurfy fetal liver, Tregs derived from IFNAR KO bone mar
14                           LV transduction of scurfy (FoxP3(mut)) HSCs restores development of functio
15                                              Scurfy (Foxp3(Sf)/Y), Il2(-/-), and Il2ralpha(-/-) mice
16 eous diabetes onset, since crossing onto the scurfy (Foxp3) mutation, BDC12-4.1 TCR Tg mice develop a
17 cally in Treg cells led to systemic, lethal, scurfy-like inflammation in mice.
18           Consistent with these results, the scurfy-like phenotype of mice lacking PDK1 in Treg cells
19  cell transfers, we tested the effect of the scurfy loss-of-function mutation of the Foxp3 gene in th
20 injury, we co-transferred isolated Tregs and Scurfy lymph node cells; Treg repletion significantly at
21                                  Transfer of scurfy lymphocytes to RAG deficient (RAG(-/-)) recipient
22 is and pneumonitis in RAG(-/-) recipients of scurfy lymphocytes.
23  dermatitis, induced by adoptive transfer of scurfy lymphocytes.
24 sed on adoptive transfer of these cells into scurfy mice (an animal model of IPEX) and a combination
25           Consistent with this, T cells from Scurfy mice (FoxP3 mutant) lacked HVEM gene expression,
26 e FOXP3, the ortholog of the gene mutated in scurfy mice (Foxp3), causes IPEX syndrome.
27 uman ortholog (FOXP3) of the gene mutated in scurfy mice (Foxp3), in IPEX patients.
28                         Mutation of Foxp3 in Scurfy mice and FOXP3 in humans with IPEX results in fat
29 autoimmune syndrome observed in Foxp3-mutant scurfy mice and Foxp3-null mice results from a CD4+CD25+
30 oimmune disease affecting multiple organs in Scurfy mice and humans with the immune dysregulation, po
31 e severity of the autoimmune diseases in the scurfy mice and in patients who have immunodysregulation
32 ells and massive multi-organ autoimmunity in scurfy mice and IPEX (immune dysregulation, polyendocrin
33 of our study indicate that autoantibodies in Scurfy mice and patients with IPEX target keratins.
34 tions substantially improved the survival of scurfy mice by blocking effector T-cell differentiation.
35 the etiology of lethal autoimmune disease in scurfy mice by stimulating the differentiation of antige
36 inatal period, germline mutation of FoxP3 in scurfy mice caused lymphopenia in the spleen and massive
37                  In this study, we show that Scurfy mice develop autoantibodies directed against skin
38                During the course of disease, Scurfy mice develop autoantibodies; however, the targete
39                                              Scurfy mice develop CD4 T-cell-mediated lymphoproliferat
40 port that removal of CD28 expression rescued scurfy mice from early death.
41 we show that Foxp3-deficient T(reg) cells in scurfy mice harboring a null mutation of the Foxp3 gene
42                                              Scurfy mice have a deletion in the Foxp3 gene, resulting
43       More importantly, T cells derived from scurfy mice have a dramatic increase in nuclear factor o
44 cells from wild-type mice or FoxP3-deficient Scurfy mice into T cell- and B cell-deficient RAG-1 knoc
45         Longer-term surviving CD28-deficient scurfy mice still had lymphoproliferative disorder, but
46                            We used DEREG and Scurfy mice to assess the role of Foxp3(+) regulatory T
47 he T reg cell compartment in Foxp3-deficient scurfy mice with cells whose ability to migrate to the s
48 rrying a loss-of-function mutation in FoxP3 (scurfy mice) present with fatal autoimmune-like disease
49 ice with naturally occurring Foxp3 mutation (Scurfy mice) substantially ameliorates clinical symptoms
50    We found that in mice deficient in Foxp3 (scurfy mice), a model of autoimmunity, the development o
51 5) knockout (KO) mice but not in IL-2 KO and scurfy mice, although all three mutants lack regulatory
52 p3 as the gene responsible for the defect in scurfy mice, and subsequently, the demonstration of its
53 ssive autoimmune syndrome similar to that of scurfy mice, but does not affect thymic development, hom
54 expansion of pathogenic T cells derived from scurfy mice, failed to mediate T follicular regulatory c
55 0 deficiency does not affect the survival of Scurfy mice, it largely abrogated the therapeutic effect
56       In most patients with IPEX and also in scurfy mice, T cells show hyperreactivity and levels of
57                                              Scurfy mice, which are deficient in a functional Foxp3,
58 e or Treg-depleted CD4 T cells in curing the scurfy mice.
59 ) and a fatal systemic autoimmune disease in scurfy mice.
60 0 induction by crossing IL-10-null allele to Scurfy mice.
61                    Although Foxp3-deficient (Scurfy) mice lacked Treg cells, they contained Triple(hi
62 CD4(+) T cell isolated from a Treg-deficient scurfy mouse.
63 ting lymphoproliferation and autoimmunity in scurfy mutant mice and immunodysregulation polyendocrino
64 of Foxp3 caused severe autoimmune disease in scurfy mutant mice, the other functional domains of Foxp
65                                          The scurfy mutation causes loss of function of the foxp3 gen
66                                          The Scurfy mutation of the FoxP3 gene (FoxP3(sf)) in the mou
67 onfirmed, as the signals were ablated by the Scurfy mutation of the FoxP3 gene.
68 pretation of our data would suggest that the scurfy mutation results in a defect, which interferes wi
69 e diabetogenic cascade, we crossed the Foxp3 scurfy mutation, which eliminates T reg cells, with the
70 d Foxp3, the gene defective in mice with the scurfy mutation.
71        Mutation of the Foxp3 gene causes the scurfy phenotype in mouse and IPEX syndrome (immune dysf
72                                  Most of the Scurfy sera tested identified a major band at 50 kDa.
73                                              Scurfy serum predominantly recognized the C-terminal fra
74   Using western blot analysis, we found that Scurfy serum reacted with proteins in total skin lysate,
75 imal mouse X chromosome containing the mouse scurfy (sf) and tattered (Td) mutations.
76 hemizygous (Xsf/Y) for the X-linked mutation scurfy (sf) develop a severe and rapidly fatal lymphopro
77                                              Scurfy (sf) is an X-linked recessive mouse mutant result
78 (OVA-specific, Vbeta5(high)Valpha2(high)) Tg scurfy (Sf) mice (OT-II Sf) that lack Treg, nonclonotypi
79                                              Scurfy (Sf) mice bear a mutation in the Foxp3 transcript
80                                              Scurfy (Sf) mice lack CD4(+)Foxp3(+) regulatory T cells
81 utation of the Foxp3 transcription factor in Scurfy (Sf) mice results in complete absence of the CD4+
82                       Therefore, we examined Scurfy (Sf) mice, animals that have a mutation in the ge
83 tion on autoimmune inflammation, we examined scurfy (Sf) mice, which are deficient in Tregs and succu
84 vation and autoimmune pathology in Foxp3(-/-)Scurfy (sf) mice.
85 MIM 304930) is the genetic equivalent of the scurfy (sf) mouse, we sequenced the human ortholog (FOXP
86 biosis and autoimmunity over the lifespan of scurfy (SF) mouse.
87 he Rag2(-/-) and the Rag2(-/-) mice with the Scurfy (sf) mutation (FoxP3(sf/Y) or FoxP3(sf/sf)) to ev
88 tudy, we investigated the reason that SMG of Scurfy (Sf), Sf.Il2(-/-), Sf.Il2ralpha(-/-), and the lon
89 ses of lymphoid cell populations reveal that scurfy syndrome is characterized by changes in several p
90                                              Scurfy T cells also exhibit strong up-regulation of cell
91 ot been identified, we also demonstrate that scurfy T cells are less sensitive than normal controls t
92                          A high frequency of scurfy T cells in TCRalpha(-/-) recipients produced IL-1
93  enhance suppressor cytokine production from scurfy T cells in TCRalpha(-/-) recipients.
94 nd B7-2, whose expression is up-regulated on scurfy T cells.
95 f the cytokine granulocyte-macrophage CSF by scurfy T cells.
96 super> T cells infiltrated the skin, whereas Scurfy Triple(lo)CD4(+) T cells induced colitis and wast