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1 on T1D that is distinct from that of any MHC class II gene.
2 ncing selection acting on MHC class I versus class II genes.
3 DR2(+) transgenic mice lacking all mouse MHC class II genes.
4 CIITA to transactivate transcription of MHC class II genes.
5 tion of the major histocompatibility complex class II genes.
6 t of proteins interact with the promoters of class II genes.
7 1, CIITA was unable to activate cellular MHC class II genes.
8 omplex are required for transcription of MHC class II genes.
9 Sjogren's syndrome are influenced by the HLA class II genes.
10 tive and IFN-gamma-induced expression of MHC class II genes.
11 on of major histocompatibility complex (MHC) class II genes.
12 ired for IFN-gamma-induced expression of MHC class II genes.
13 IITA) activates the transcription of all MHC class II genes.
14 constitutive and inducible expression of MHC class II genes.
15 rm of RNA polymerase activates expression of Class II genes.
16 for CIITA to function as an activator of MHC class II genes.
17 dependent diabetes mellitus is linked to MHC class II genes.
18 FIIB) play crucial roles in transcription of class II genes.
19 equired for the functional regulation of MHC class II genes.
20 mune response to insulin is regulated by MHC class II genes.
21 A splicing and transcriptional activation of class II genes.
22 ements and is required for expression of MHC class II genes.
23 in NF-Y-mediated transcriptional control of class II genes.
24 ys an important role in the transcription of class II genes.
25 f the major histocompatibility complex (MHC) class II genes.
26 re a common mechanism of regulation with the class II genes.
27 o not bind to the homologous sequence of all class II genes.
28 and CIITA are responsible for activation of class II genes.
29 ding proteins that functionally regulate MHC class II genes.
30 ory factors controlling transcription of MHC class II genes.
31 moters and is essential for transcription of class II genes.
32 synonymous substitution in the PBR of mouse class II genes.
33 romoters of major histocompatibility complex class II genes.
34 human major histocompatibility complex (MHC) class II genes.
35 quired for IFN-gamma-inducible expression of class II genes.
36 m a coordinated lack of transcription of all class II genes.
37 pression or major histocompatibility complex class II genes.
38 to be strongly associated with specific HLA class II genes.
39 ion complex genes, and were depleted for MHC class II genes.
40 histocompatibility complex region, near HLA class II genes.
41 nscriptional coactivator CIITA regulates MHC class II genes.
42 pression of major histocompatibility complex class II genes.
43 kappaB1, and SP1 sites were more enriched in class II genes.
44 n to the established associations of the MHC class II genes.
45 s the master integrator of expression of MHC class II genes.
46 in the reciprocal-suppressive effect between class II genes.
47 on factor required for the expression of MHC class II genes.
48 X1 box sequence located upstream of all MHC class II genes.
49 by sequencing TAP1, in conjunction with HLA class II genes.
50 nuclear translocation and expression of MHC class II genes.
51 r (CIITA) is the 'master coactivator' of MHC class II genes.
52 ater than that of mutation in the history of class II genes.
53 variation in the IL4RA gene (16p12), the HLA class II genes (6p21), and the interferon-alpha gene clu
54 M genes are regulated in a similar manner as class II genes, a series of in vivo and in vitro analyse
55 imum amount of IFN-gamma is required for MHC class II gene activation despite the fact that the level
56 s generated that lacked all endogenous mouse class II genes (AE(o)) and expressed the RA susceptibili
57 r map of chicken MHC genes (containing a MHC class II gene and two rRNA genes) to Rfp-Y validated the
59 ations between human leukocyte antigen (HLA) class II genes and both rubella-specific immunoglobulin
60 1.DQ8 mice, activated CD4(+) T cells express class II genes and can present DR4- and DQ8-restricted p
61 e classical major histocompatibility complex class II genes and cytotoxic T cell antigen-4, new studi
63 , including major histocompatibility complex class II genes and genes in human hepatitis B virus.
64 loenzyme is essential for expression of most class II genes and is a target of at least one transcrip
65 ential for transcriptional activation of MHC class II genes and mediates enhanced MHC class I transcr
66 itment to proximal promoter sequences in MHC class II genes and more distally involving the canonical
67 vator (CIITA) is a critical regulator of MHC class II genes and other genes involved in the Ag presen
68 , including major histocompatibility complex class II genes and other genes located within this regio
69 dently of CIITA, the master regulator of MHC class II genes and prepare the MHC for subsequent induct
70 RFX complex to DNA, transcription of all MHC class II genes and the appearance of these determinants
71 f the highly polymorphic HLA class I and HLA class II genes and the complex structural diversity of c
72 Elucidation of functionally important dog class II genes and the identification of 23 microsatelli
74 echanism for the uncoupled regulation of MHC class II genes and the processing enzyme GILT in human m
76 y flagellar basal body structure, encoded by class II genes, and is activated by the transcription fa
77 hown to transactivate MHC class I as well as class II genes, and this investigation shows that CIITA
78 . aeruginosa infection were enriched for HLA class II genes, and those associated with MI were relate
79 of the HLA-DRA gene, the canonical human MHC class II gene; and with increased Rb binding to the YY1
80 pulates that Class I genes are repressed and Class II genes are activated by high levels of Shh signa
82 eneic major histocompatibility complex (MHC) class II genes are cell-based vaccines for the treatment
87 ly expressed in the subjective dusk, whereas class II genes are maximally expressed in the subjective
88 ss, there is substantial evidence that human class II genes are not always coordinately regulated, ra
89 Because small numbers of MHC class I and class II genes are present in both B: and Rfp-Y, the two
95 enetically modified to express syngeneic MHC class II genes as cell-based immunogens and is based on
97 und to be required for expression of all MHC class II genes associated with antigen presentation.
100 role in development, we demonstrate that the class II gene AtTPS6 is important for controlling cellul
101 ma was required for strong overexpression of class II genes but not for CD4(+) T cell activation, oli
102 , CIITA not only activates the expression of class II genes but recruits another B cell-specific coac
105 ctivator that directly controls development (class II) genes by binding to the DAF-16-associated elem
106 ial proximity between PML bodies and the MHC class II gene cluster in different human cell types.
110 l sex workers had individual alleles for HLA class II genes determined by using labeled sequence-spec
113 tides corresponding to the X2 box of the MHC class II genes DPA and DQB were used to screen B cell an
115 ells of these patients do not transcribe MHC class II genes due to a defect in the trans-acting facto
116 expression of IFN-gamma-inducible genes-MHC class II gene E beta; MHC class II transactivator; IFN r
117 llitus in humans is linked with specific HLA class II genes, e.g., HLA-DQA1*0301/ DQB1*0302 (DQ8).
118 g the major histocompatibility complex (MHC) class II genes (eg, HLA-DRA) which correlated with bette
119 The major histocompatibility complex (MHC) class II genes encode a series of heterodimeric cell sur
120 s code for regulatory components of closure: Class II genes encode Drosophila Jun amino (N)-terminal
122 activity can repress IFN-gamma-inducible HLA class II gene expression and also demonstrate that HDAC
123 ontrol of CIITA is necessary to regulate MHC class II gene expression and induction of an immune resp
124 )-inducible major histocompatibility complex class II gene expression and transcriptionally productiv
126 gulation of major histocompatibility complex class II gene expression as well as in exocrine gland an
128 or (CIITA) is known as a coactivator for MHC class II gene expression in antigen-presenting cells.
130 equences of Shh misexpression on Class I and Class II gene expression in the hindbrain of ShhP1 embry
131 ritical for major histocompatibility complex class II gene expression in vivo contribute to both the
134 activator (CIITA), is a key regulator of MHC class II gene expression that associates and cooperates
135 DQ8 transgenic mice lacking endogenous mouse class II gene expression were actively immunized and lat
136 is domain contributes to MHC class I and MHC class II gene expression with a bias for activation of M
137 ss of major histocompatibility complex (MHC) class II gene expression, is caused by inherited mutatio
142 highly conserved WXY motifs, and, like other class II genes, expression of both DN alpha and DO beta
143 III anti-sigma28 gene, flgM, flanked by the class II genes, flgA, flgBCD and flhBA, and a novel puta
144 We examined intron phase I-containing HLA class II genes for the presence of intergenic mRNAs and
145 suggest that the conserved X and Y boxes of class II genes function similarly and define a single mu
146 de from a few common human leukocyte antigen class II genes--had been identified that clearly associa
148 the 5' proximal promoter region of the human class II gene HLA-DQA1 have been shown to influence its
150 ity determinants have been mapped to the MHC class II genes HLA-DQB1 and HLA-DRB1, but these genes ca
157 et autoantibodies localizing to the same HLA class II genes, HLA-DRB1 and HLA-DQB1, the effects of th
159 h regard to the coordinate regulation of the class II genes if the factors though to regulate the HLA
160 current study we studied the HLA class I and class II genes in 231 Chinese voluntary blood donors who
161 n histocompatibility leukocyte antigen (HLA) class II genes in 54 cases of tuberculoid leprosy (TL) a
162 consistent and strong associations with MHC class II genes in Caucasian patients with inflammatory b
163 mice has helped to elucidate the role of HLA class II genes in chronic inflammatory and demyelinating
164 To investigate the role of individual HLA class II genes in immune responses to human Ro60 (hRo60)
165 s Ciita and major histocompatibility complex class II genes in murine macrophages, thereby inhibiting
167 Furthermore, IFN-gamma induction of the MHC class II genes in solid human tumor lines requires retin
168 ins encoded by the classical HLA class I and class II genes in the major histocompatibility complex (
169 ces the activator-dependent transcription of class II genes in vitro, but it was later shown that PC4
170 is generally required for activation of all class II genes in vivo, we have constructed substitution
172 s are independent of human leukocyte antigen class II genes in whites but may interact antagonistical
175 tivator (CIITA) is a master regulator of MHC class II genes, including DR, DP, and DQ, and MHC class
176 investigating the transfer of allogeneic MHC class II genes into recipient bone marrow cells (BMC), u
178 al human leukocyte antigen (HLA) Class I and Class II genes is among the most polymorphic and diverse
180 o inherit putative protective alleles of HLA class II genes is linked to the development of breast ca
181 The expression of major histocompatibility class II genes is necessary for proper antigen presentat
182 ences present in the promoters of eukaryotic class II genes is the first step in the sequential assem
183 of the reciprocal-suppressive effect between class II genes is unclear, although the involvement of r
184 The transcription of nonconventional MHC class II genes is, however not affected by CIITA deficie
185 of C57BL/6 major histocompatibility complex class II gene knockout mice and CD4 cell-depleted C3H mi
186 ( P = 7.5 x 10(-35)), which included the HLA class II genes, known to be the primary determinants of
187 In the present study, we characterize an MHC class II gene-linked butyrophilin family member, butyrop
188 ns in major histocompatibility complex (MHC) class II genes may be of pathogenetic importance in infl
189 ith type 1 diabetes independently of the MHC class II genes (MICA P = 0.08, MICA-STR P = 0.76, MICB P
190 n histocompatibility leukocyte antigen (HLA) class II gene most commonly associated with human type 1
191 latory sequences are conserved among all MHC class II genes, multiple base pair changes are found, ev
195 e TAP1 gene to human leukocyte antigen (HLA) class II genes on chromosome 6, we postulated that a lin
196 ce to eliminate any effect of endogenous MHC class II genes on the development of autoimmune diseases
199 major histocompatibility complex class I and class II gene products and certain chemokine genes are t
201 s (Abo) were used to investigate the role of class II gene products in resistance or susceptibility t
202 histocompatibility complex (MHC) class I and class II gene products in the development of functional
206 atory factors required for expression of MHC class II genes, rather than the genes themselves, are re
210 , encompassing two MHC class I and three MHC class II genes, separated from the B system by a region
214 ciation of type 1 diabetes with specific MHC class II genes, such as I-A(g7) in nonobese diabetic mic
216 Our findings demonstrate that BAD1 is a TCP class II gene that functions to promote cell proliferati
217 s III regions, including the MHC class I and class II genes that play a primary role in the immune re
220 ecent data from the author's laboratory on a class II gene therapy induction of tolerance to allogene
222 Thus, hTRFP may regulate transcription of class II genes through association with the RNA polymera
223 response (class I) and downregulating other (class II) genes through a mechanism that depends on the
225 on also reduces transcription of seven other class II genes, thus indicating a broad role for this yT
228 likely responsible for this higher level of class II gene transcription, as purified Tax was found t
234 n that transplantation tolerance, induced by class II gene transfer into syngeneic BMC, results in pa
235 ese results demonstrate the potential of MHC class II gene transfer to permit tolerance to solid orga
236 nism of tolerance induction achieved through class II gene transfer, BMC from C57BL/10 mice, which la
237 e mice were generated by introduction of HLA class II genes, various human cytokines, and human B cel
238 nkage of ring3 and beta2M to MHC class I and class II genes was determined by single-strand conformat
240 as NO insensitive in vitro, transcription of class II genes was moderately induced by NO, which invol
243 uniformly induced by p53 in all cell lines; "class II" genes were induced in a subset of the lines; a
244 n levels of major histocompatibility complex class II genes, whereas a differential ubiquitin signatu
245 ator of the major histocompatibility complex class II genes, which are involved in antigen presentati
246 s the expression of major histocompatibility class II genes, which encode antigen-presenting molecule
247 c, the stretches that encode the class I and class II genes, which epitomize the Mhc, are the least c
248 ern of dyscoordinate regulation of their MHC class II genes, which is reflected in a new phenotype of
249 a CIITA-inducible gene, and DO beta as a MHC class II gene whose expression is independent of CIITA.
250 port in live APCs, we replaced the mouse MHC class II gene with a version that codes for a class II m
252 gene mutations, including 8 class I genes, 4 class II genes, WT1 and TP53 (class III), and 5 epigenet
253 , binds to the promoter regions of flagellar class II genes, yet, despite extensive analysis of the F
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