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1 ion on T1D that is distinct from that of any MHC class II gene.
2 dhesion complex genes, and were depleted for MHC class II genes.
3 transcriptional coactivator CIITA regulates MHC class II genes.
4 titutive and IFN-gamma-induced expression of MHC class II genes.
5 ition to the established associations of the MHC class II genes.
6 A) is the master integrator of expression of MHC class II genes.
7 iption factor required for the expression of MHC class II genes.
8 rved X1 box sequence located upstream of all MHC class II genes.
9 the nuclear translocation and expression of MHC class II genes.
10 vator (CIITA) is the 'master coactivator' of MHC class II genes.
11 HLA-DR2(+) transgenic mice lacking all mouse MHC class II genes.
12 y of CIITA to transactivate transcription of MHC class II genes.
13 BRG-1, CIITA was unable to activate cellular MHC class II genes.
14 NF complex are required for transcription of MHC class II genes.
15 required for IFN-gamma-induced expression of MHC class II genes.
16 r (CIITA) activates the transcription of all MHC class II genes.
17 ulatory factors controlling transcription of MHC class II genes.
18 oth constitutive and inducible expression of MHC class II genes.
19 red for CIITA to function as an activator of MHC class II genes.
20 lin-dependent diabetes mellitus is linked to MHC class II genes.
21 ns required for the functional regulation of MHC class II genes.
22 e immune response to insulin is regulated by MHC class II genes.
23 E elements and is required for expression of MHC class II genes.
24 -binding proteins that functionally regulate MHC class II genes.
25 ression of major histocompatibility complex (MHC) class II genes.
26 ion of the major histocompatibility complex (MHC) class II genes.
27 with human major histocompatibility complex (MHC) class II genes.
28 minimum amount of IFN-gamma is required for MHC class II gene activation despite the fact that the l
29 cular map of chicken MHC genes (containing a MHC class II gene and two rRNA genes) to Rfp-Y validated
30 essential for transcriptional activation of MHC class II genes and mediates enhanced MHC class I tra
31 ecruitment to proximal promoter sequences in MHC class II genes and more distally involving the canon
32 activator (CIITA) is a critical regulator of MHC class II genes and other genes involved in the Ag pr
33 ependently of CIITA, the master regulator of MHC class II genes and prepare the MHC for subsequent in
34 the RFX complex to DNA, transcription of all MHC class II genes and the appearance of these determina
36 ar mechanism for the uncoupled regulation of MHC class II genes and the processing enzyme GILT in hum
37 ulation of Major Histocompatibility Complex (MHC)class II genes and an effective immune response.
38 ter of the HLA-DRA gene, the canonical human MHC class II gene; and with increased Rb binding to the
41 syngeneic major histocompatibility complex (MHC) class II genes are cell-based vaccines for the trea
43 ls genetically modified to express syngeneic MHC class II genes as cell-based immunogens and is based
44 s found to be required for expression of all MHC class II genes associated with antigen presentation.
45 spatial proximity between PML bodies and the MHC class II gene cluster in different human cell types.
48 cleotides corresponding to the X2 box of the MHC class II genes DPA and DQB were used to screen B cel
49 he cells of these patients do not transcribe MHC class II genes due to a defect in the trans-acting f
50 uced expression of IFN-gamma-inducible genes-MHC class II gene E beta; MHC class II transactivator; I
51 luding the major histocompatibility complex (MHC) class II genes (eg, HLA-DRA) which correlated with
53 ct control of CIITA is necessary to regulate MHC class II gene expression and induction of an immune
55 ivator (CIITA) is known as a coactivator for MHC class II gene expression in antigen-presenting cells
58 ransactivator (CIITA), is a key regulator of MHC class II gene expression that associates and coopera
59 t this domain contributes to MHC class I and MHC class II gene expression with a bias for activation
63 to loss of major histocompatibility complex (MHC) class II gene expression, is caused by inherited mu
64 ibility determinants have been mapped to the MHC class II genes HLA-DQB1 and HLA-DRB1, but these gene
67 e of consistent and strong associations with MHC class II genes in Caucasian patients with inflammato
70 l activator (CIITA) is a master regulator of MHC class II genes, including DR, DP, and DQ, and MHC cl
71 are investigating the transfer of allogeneic MHC class II genes into recipient bone marrow cells (BMC
74 In the present study, we characterize an MHC class II gene-linked butyrophilin family member, but
75 iations in major histocompatibility complex (MHC) class II genes may be of pathogenetic importance in
76 CB with type 1 diabetes independently of the MHC class II genes (MICA P = 0.08, MICA-STR P = 0.76, MI
77 regulatory sequences are conserved among all MHC class II genes, multiple base pair changes are found
79 ) mice to eliminate any effect of endogenous MHC class II genes on the development of autoimmune dise
81 egulatory factors required for expression of MHC class II genes, rather than the genes themselves, ar
83 fp-Y, encompassing two MHC class I and three MHC class II genes, separated from the B system by a reg
84 association of type 1 diabetes with specific MHC class II genes, such as I-A(g7) in nonobese diabetic
85 scriptionally a more potent activator of the MHC class II gene than the form expressed in B cells.
91 These results demonstrate the potential of MHC class II gene transfer to permit tolerance to solid
93 pattern of dyscoordinate regulation of their MHC class II genes, which is reflected in a new phenotyp
94 as a CIITA-inducible gene, and DO beta as a MHC class II gene whose expression is independent of CII
95 ransport in live APCs, we replaced the mouse MHC class II gene with a version that codes for a class
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