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1 fy beta2-microglobulin (B2M), a component of major histocompatibility complex class 1 (MHC I) molecul
4 is nonbiased approach has revealed Raet1e, a major histocompatibility complex class 1-like molecule e
6 potential role of the vaccine in conferring major histocompatibility complex class 1-mediated protec
7 M subtypes for their ability to downregulate major histocompatibility complex class A (MHC-A) and MHC
8 rials used for particulate immunotherapy, in major histocompatibility complex class I (MHC I) and MHC
9 tance to toxoplasmic encephalitis in mice to major histocompatibility complex class I (MHC I) and ult
10 oading complex (PLC) is required for optimal major histocompatibility complex class I (MHC I) antigen
11 6 was markedly more effective at suppressing major histocompatibility complex class I (MHC I) display
12 provided comparable protection in wild-type, major histocompatibility complex class I (MHC I) knockou
13 our cells depends on antigen presentation by major histocompatibility complex class I (MHC I) molecul
14 presentation to cytotoxic T lymphocytes via major histocompatibility complex class I (MHC I) molecul
17 sing Indian rhesus macaques that express the major histocompatibility complex class I (MHC-I) allele
20 The best-characterized targets of Nef are major histocompatibility complex class I (MHC-I) and CD4
21 xpression of a spectrum of peptides bound to major histocompatibility complex class I (MHC-I) and cla
22 ulation of immune synapse components such as major histocompatibility complex class I (MHC-I) and ICA
23 ER) that abrogates cell surface transport of major histocompatibility complex class I (MHC-I) and MHC
24 evels of expression of genes associated with major histocompatibility complex class I (MHC-I) and MHC
25 calized chaperone facilitating maturation of major histocompatibility complex class I (MHC-I) and the
26 nimals used in the study suggested that host major histocompatibility complex class I (MHC-I) and TRI
27 correlates with generalized up-regulation of major histocompatibility complex class I (MHC-I) antigen
28 ll immunity by virally encoded inhibitors of major histocompatibility complex class I (MHC-I) antigen
29 n that functions by enhancing degradation of major histocompatibility complex class I (MHC-I) antigen
30 0I, unexpectedly and uniquely degraded Nef's major histocompatibility complex class I (MHC-I) downreg
31 LCMV V35A) bearing a mutation in the cognate major histocompatibility complex class I (MHC-I) epitope
33 Flow cytometry analyses showed decreased major histocompatibility complex class I (MHC-I) express
34 inactivating mutations that lead to loss of major histocompatibility complex class I (MHC-I) express
35 s with varied binding affinities to specific major histocompatibility complex class I (MHC-I) haploty
38 ocess and present extracellular antigen with major histocompatibility complex class I (MHC-I) molecul
40 downregulation of the surface expression of major histocompatibility complex class I (MHC-I) molecul
41 roteins that prevent antigen presentation by major histocompatibility complex class I (MHC-I) molecul
42 eficiency viruses (HIV and SIV) downregulate major histocompatibility complex class I (MHC-I) molecul
44 ins that modulate cell surface expression of major histocompatibility complex class I (MHC-I) molecul
45 ctly or indirectly upregulate both PD-L1 and major histocompatibility complex class I (MHC-I) on mous
46 lymphocytes through constitutively expressed major histocompatibility complex class I (MHC-I) or CD4(
47 alleles, macaques express up to 20 distinct major histocompatibility complex class I (MHC-I) sequenc
48 inst NS5 were also elicited, as evidenced by major histocompatibility complex class I (MHC-I) tetrame
49 us type 12 (Ad12) involves downregulation of major histocompatibility complex class I (MHC-I) transcr
52 e HIV Nef protein on antigen presentation by major histocompatibility complex class I (MHC-I), and ev
53 ts of rodent neurons are reported to express major histocompatibility complex class I (MHC-I), but su
55 iency virus type 1 (HIV-1) Nef downregulates major histocompatibility complex class I (MHC-I), impair
56 nt molecules involved in these events is the Major Histocompatibility Complex class I (MHC-I), respon
57 IR1 has been shown to primarily downregulate major histocompatibility complex class I (MHC-I), wherea
58 cells kill SIV-infected CD4(+) T cells in an major histocompatibility complex class I (MHC-I)-depende
59 The NKR-P1B:Clr-b interaction represents a major histocompatibility complex class I (MHC-I)-indepen
62 al immune evasion is the capacity to disrupt major histocompatibility complex class I (MHCI) antigen
68 n subjects with ALS reduce the expression of major histocompatibility complex class I (MHCI) molecule
71 iated immunity is the recognition of peptide-major histocompatibility complex class I (p-MHC I) prote
73 ow cytometry for donor-specific chimerism of major histocompatibility complex class I (RT1) antigen,
74 pe mutations into 30 epitopes (bound by five major histocompatibility complex class I [MHC-I] molecul
75 , the three controller macaques each carried major histocompatibility complex class I alleles that pr
79 tion, antigen presentation, and detection of major histocompatibility complex class I and II-presente
80 blood mononuclear cell DEGs associated with major histocompatibility complex class I and natural kil
81 n lead to reduced cell surface expression of major histocompatibility complex class I and tumor necro
82 otein complex that normally functions during major histocompatibility complex class I biogenesis in t
84 al cells (ECs) expressed antigens, including major histocompatibility complex class I chain-related a
85 it interacts with two groups of ligands: the major histocompatibility complex class I chain-related A
86 e same points of time were assessed for HLA, major histocompatibility complex class I chain-related g
87 assified as either alloantigens, such as the major histocompatibility complex class I chain-related g
88 rmal controls, and the clinical relevance of major histocompatibility complex class I chain-related g
89 , killer-cell immunoglobulin-like receptors, major histocompatibility complex Class I chain-related g
90 er-cell immunoglobulin-like receptors (KIR), major histocompatibility complex class I chain-related g
92 erefore, the identification of antigens with major histocompatibility complex class I epitopes is a c
93 ne profile with significantly more prominent major histocompatibility complex class I expression and
96 features of perifascicular fiber atrophy and major histocompatibility complex class I expression.
97 cific CD8(+) T-cell responses as measured by major histocompatibility complex class I Gag-tetramer st
99 cient US2- and US11-dependent dislocation of major histocompatibility complex class I heavy chains.
100 ity control to facilitate the destruction of major histocompatibility complex class I heavy chains.
101 Culture of aortic rings with antibody to major histocompatibility complex class I inhibited endot
102 the presentation of these envelope motifs by major histocompatibility complex class I is enhanced by
103 ike receptor (iKIR) for which the respective major histocompatibility complex class I ligand is absen
104 bitory receptors on F1 NK cells and parental major histocompatibility complex class I ligands determi
105 usly generating peptides that could serve as major histocompatibility complex class I ligands, markin
106 nto the endoplasmic reticulum (ER) lumen for major histocompatibility complex class I loading and cel
107 sponse mediates endothelial dysfunction in a major histocompatibility complex class I mismatch model.
108 ween monkeys that share the same restricting major histocompatibility complex class I molecule and re
112 on at the surface of most nucleated cells by major histocompatibility complex class I molecules (MHC
113 ed by the interaction of Ly49 receptors with major histocompatibility complex class I molecules (MHC-
115 mor growth of melanoma cell lines expressing major histocompatibility complex class I molecules at hi
116 g function that influences the expression of major histocompatibility complex class I molecules at th
117 expressing human HLA-A2.1 but lacking murine major histocompatibility complex class I molecules devel
118 this study, we evaluated the contribution of major histocompatibility complex class I molecules to br
119 lasmic reticulum and subsequent loading onto major histocompatibility complex class I molecules to tr
120 culin to mediate assembly and trafficking of major histocompatibility complex class I molecules, whic
121 CTLs by inducing large amounts of noncognate major histocompatibility complex class I molecules, whic
122 ible for the generation of peptides bound to major histocompatibility complex class I molecules.
123 NK cells migrate to the tumor site to reject major histocompatibility complex class I negative tumors
124 ector lymphocytes that control the growth of major histocompatibility complex class I negative tumors
125 epatitis B virus (HBV) epitopes presented by major histocompatibility complex class I on infected cel
126 to such allografts that lacked expression of major histocompatibility complex class I or II molecules
128 lex, non-DRB1 loci, a polymorphism marker in major histocompatibility complex class I polypeptide-rel
131 viral persistence in part by down-regulating major histocompatibility complex class I protein (MHC-I
132 whereas other CIE cargo proteins, including major histocompatibility complex class I protein (MHCI),
134 usceptible to cytotoxic, gp100 reactive, and major histocompatibility complex class I restricted CD8(
135 ubjects (n = 27) using overlapping peptides, major histocompatibility complex class I tetramers, and
136 hich depletes endoplasmic reticulum calcium, major histocompatibility complex class I trafficking rat
137 ent pairs were selected based on ABO typing, major histocompatibility complex class I typing, and car
139 In contrast, another CIE cargo protein, major histocompatibility complex class I, which normally
140 esponsiveness requires positive selection on major histocompatibility complex class I-associated pept
141 1) rapidly and efficiently downregulates the major histocompatibility complex class I-like antigen-pr
143 ults from defects in the HFE gene product, a major histocompatibility complex class I-like protein th
144 tial facial segment allotransplantation from major histocompatibility complex class I-mismatched dono
145 -MHC antibodies, including those recognising major histocompatibility complex class I-related chain A
146 NKG2D on NK cells and the hepatocyte protein major histocompatibility complex class I-related chains
148 on of bacterial metabolites presented by the major histocompatibility complex class I-related molecul
149 ic CD8(+) T cells with increased avidity for major histocompatibility complex class I-restricted Gag
154 inflammatory responses as well as increased major histocompatibility complex class I/II expression b
156 469 located on 6p22.1, and covering lncRNAs (major histocompatibility complex, class I, A (HLA-A) and
159 ous cell carcinoma-1 (NY-ESO-1) proteins and major-histocompatibility-complex-class-I-tetramers speci
160 eract with peptides bound to the polymorphic major histocompatibility complex class Ia (MHC-Ia) and c
161 w that soluble molecules of the nonclassical major histocompatibility complex class Ib (MHC-Ib) antig
162 en, characterized by increased expression of major histocompatibility complex class II (approximately
163 rces capture of pathogen-derived epitopes by major histocompatibility complex class II (MHC class II)
164 Although unusual neutrophils expressing major histocompatibility complex class II (MHC II) and c
165 e developed a mouse strain that lacks murine major histocompatibility complex class II (MHC II) and i
166 hy adult human liver expresses low levels of major histocompatibility complex class II (MHC II) and u
168 nduced upregulation of CD80, CD86, CD40, and major histocompatibility complex class II (MHC II) expre
169 their ability to bind promiscuously to human major histocompatibility complex class II (MHC II) molec
170 Here we have shown that eTACs are a discrete major histocompatibility complex class II (MHC II)(hi),
172 sential for error-free lineage choice during major histocompatibility complex class II (MHC II)-speci
173 l for selected genes, including those of the major histocompatibility complex class II (MHC II).
174 ion of Ifnbeta, Ccl5, and Cxcl10 and surface major histocompatibility complex class II (MHC-II) and M
176 Inoculation with M. canis also decreased major histocompatibility complex class II (MHC-II) antig
178 ng been known that T. gondii interferes with major histocompatibility complex class II (MHC-II) antig
179 Expression of vIRF3 downregulates surface major histocompatibility complex class II (MHC-II) DR ex
180 in WT-infected mice as measured by CD11b and major histocompatibility complex class II (MHC-II) expre
181 r (CIITA) is essential for the expression of major histocompatibility complex class II (MHC-II) genes
184 for assembly of cargo-derived peptides with major histocompatibility complex class II (MHC-II) molec
188 eins, called epitopes, that are presented by major histocompatibility complex class II (MHC-II) molec
189 en presentation in addition to the classical major histocompatibility complex class II (MHC-II) pepti
190 lly decreases the degradative processing and major histocompatibility complex class II (MHC-II) prese
192 ific for mouse CMV (MCMV) epitopes and use a major histocompatibility complex class II (MHC-II) tetra
193 t the activation of CD4 via interaction with major histocompatibility complex class II (MHC-II) trigg
194 on and antigen presentation, including CD69, major histocompatibility complex class II (MHC-II), and
195 ll mutant stimulates the expression of CD86, major histocompatibility complex class II (MHC-II), and
196 hese noninfected DC showed downregulation of major histocompatibility complex class II (MHC-II), CD40
197 activated/mature, expressing lower levels of major histocompatibility complex class II (MHC-II), CD86
198 ein superantigen presented in the context of major histocompatibility complex class II (MHC-II), whic
199 ncodes the beta subunit of the non-classical major histocompatibility complex class II (MHC-II)-like
200 for viral entry but without interfering with major histocompatibility complex class II (MHC-II)-media
201 elucidating several previously unidentified major histocompatibility complex class II (MHC-II)-restr
202 ologous antigen-specific CD4(+) T cells in a major histocompatibility complex class II (MHC-II; HLA-D
204 yses revealed that RORgammat(+) ILCs express major histocompatibility complex class II (MHCII) and ca
205 led to a transient increase in expression of major histocompatibility complex class II (MHCII) and CD
206 se to alpha-syn fibrils, with attenuation of major histocompatibility complex class II (MHCII) and pr
207 on rechallenge, with protection dependent on major histocompatibility complex class II (MHCII) expres
208 lymphoid cell (ILC3)-intrinsic expression of major histocompatibility complex class II (MHCII) is reg
210 ate in DC-to-MC molecule transfers including major histocompatibility complex class II (MHCII) protei
211 acterizations of classical and non-classical major histocompatibility complex class II (MHCII) protei
212 ntain a highly dynamic pool of intracellular major histocompatibility complex class II (MHCII) that c
213 enes including cyclo-oxygenase-2 (COX-2) and major histocompatibility complex class II (MHCII), induc
214 utoimmune-disease-relevant peptides bound to major histocompatibility complex class II (pMHCII) molec
215 Tregs are not required to directly recognize major histocompatibility complex class II alloantigens t
216 We examined parenchymal rejection after major histocompatibility complex class II allomismatched
217 gin when naive CD4(+) T cells engage peptide+major histocompatibility complex class II and co-stimula
218 n likely due to reduced expression levels of major histocompatibility complex class II and costimulat
219 ated with PFD showed decreased expression of major histocompatibility complex class II and costimulat
221 eract with T cells was assessed by measuring major histocompatibility complex class II and costimulat
222 strains tested induced surface expression of major histocompatibility complex class II and costimulat
223 reduced, with decreased brain expression of major histocompatibility complex class II and glial fibr
224 ent with AZD1480 inhibited alpha-SYN-induced major histocompatibility complex Class II and inflammato
225 rimed yet expected phenotype, with increased major histocompatibility complex class II and lower phag
226 AMs by their strong expression of CD11b and major histocompatibility complex class II and modest exp
227 uction of Treg cells by normal CMFs required major histocompatibility complex class II and prostaglan
228 (SEB) is a superantigen that cross-links the major histocompatibility complex class II and specific V
230 UW-3/Cx) to induce infertility in mice whose major histocompatibility complex class II antigen was re
231 with an increased number of macrophages and major histocompatibility complex class II antigen-presen
232 ed 44 epitopes that are predicted to be good major histocompatibility complex class II binders and at
234 severe combined immunodeficiency (ADA-SCID), major histocompatibility complex class II deficiency] an
235 , and this is mediated, at least in part, by major histocompatibility complex class II distribution o
236 ority of cattle, although three animals with major histocompatibility complex class II DRB3 restricti
237 markers (CD40, DC80, and CD86), and reduced major histocompatibility complex class II expression in
238 lls and monocytes was contact dependent, and major histocompatibility complex class II expression may
240 ed by a pathway requiring cell-cell contact, major histocompatibility complex class II expression on
241 targeting class II transactivator attenuates major histocompatibility complex class II expression on
242 ion, as determined by macrophage content and major histocompatibility complex class II expression, sh
243 or X, two transcription factors dedicated to major histocompatibility complex class II expression, su
244 FX5(N) (62-LYLYLQL-68) that are critical for major histocompatibility complex class II gene expressio
245 d secondary response genes such as Ciita and major histocompatibility complex class II genes in murin
246 monocytes show highest expression levels of major histocompatibility complex class II genes, whereas
250 teria, had stronger myocardial expression of major histocompatibility complex class II molecule and e
251 lysis shows that WE14 bound to the NOD mouse major histocompatibility complex class II molecule I-A(g
252 e of the alpha- and beta-chains of the human major histocompatibility complex class II molecule.
254 esenting a high density of peptides bound to major histocompatibility complex class II molecules (pMH
255 nfection most effectors require signals from major histocompatibility complex class II molecules and
256 enabled the presentation of self antigens by major histocompatibility complex class II molecules in a
257 in the infused protein and the competence of major histocompatibility complex class II molecules to p
258 l processing and presentation of peptides on Major Histocompatibility Complex class II molecules, as
260 tosed antigens for prolonged presentation on major histocompatibility complex class II molecules.
261 om internalized antigens in combination with major histocompatibility complex class II molecules.
262 lineage, despite the presence of polymorphic major histocompatibility complex class II molecules.
263 oximately 30-50%) in expression of CD11b and major histocompatibility complex class II on both monocy
264 gen-presenting cells and presentation by the major histocompatibility complex class II pathway to CD4
266 ; and that these CD4(-) T cells can maintain major histocompatibility complex class II restriction.
267 fect is not solely due to linkage with known major histocompatibility complex class II susceptibility
268 ation of VZV-specific CD4(+) T cells with an major histocompatibility complex class II tetramer (epit
270 CD4(+) T cells, below detection with peptide-major histocompatibility complex class II tetramers, wer
271 eptides, and peptide presentation on nascent major histocompatibility complex class II to T cells.
273 pathology by quantifying the infiltration of major histocompatibility complex class II(+) (I-A(d+)) d
274 associated with increased CD68(+) (P=0.002), major histocompatibility complex class II(+) (P=0.002),
275 CD68(+) (P=0.009 and P=0.008, respectively), major histocompatibility complex class II(+) (P=0.003 an
276 vitro studies confirmed that mature CCR7(+) major histocompatibility complex class II(+) CD86(+) gra
277 -10 messenger RNA and CD8(+)CD11c(+)CD205(+) major histocompatibility complex class II(+) dendritic c
278 ction of both dendritic cells (DCs; CD11c(+) major histocompatibility complex class II(+)) and alveol
280 e heterogeneity of medial cells (measured by major histocompatibility complex class II) after carotid
281 ontent (CD68), activated inflammatory cells (major histocompatibility complex class II), and microves
282 first 2 h and were instead found in LAMP2+, major histocompatibility complex class II+ (MHC-II+) H2-
283 ive CD4 T cells were competent to lyse donor major histocompatibility complex class II+ target cells,
286 -cell receptor+ cells that express CD11c and major histocompatibility complex class II, and require F
287 ific differences in expression of microglial major histocompatibility complex class II, C-C chemokine
288 ating factor, and intragraft transcripts for major histocompatibility complex class II, Toll-like rec
289 can cross-link the T cell receptor (TCR) and major histocompatibility complex class II, triggering a
291 cluded restoration of mature macrophages and major histocompatibility complex class II-expressing den
292 nly a single NR2A or NR2B C-terminal domain, major histocompatibility complex class II-NR2A homodimer
293 ers of CD4 T cells and a large population of major histocompatibility complex class II-restricted CD8
294 lysosomal thiol reductase (GILT) facilitates major histocompatibility complex class II-restricted pro
295 ssed LMO2, CD58, and stromal-1-signature and major histocompatibility complex class II-signature gene
296 eins in the endogenous Cd8 gene locus caused major histocompatibility complex class II-specific thymo
297 ed lesion expression of inflammatory markers major histocompatibility complex-class II and IL6, lesio
298 IFNs, IL-6, and TNF-alpha nor expression of major-histocompatibility-complex class II or costimulato
299 nic effect on AML cells in vivo upregulating major histocompatibility complex class-II, costimulatory
300 he variable nature of this protein, a common major histocompatibility complex class (MHC-II) epitope
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