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1 dictating the internalization and subsequent MHC class I (MHC I) display of extracellular Ags.
2  express inhibitory receptors that bind self-MHC class I (MHC I) molecules and prevent killing of sel
3 esented by classical as well as nonclassical MHC class I (MHC I) molecules is altered in the absence
4                                              MHC class I (MHC-I) molecules are the centerpieces of cr
5                       Binding of peptides to MHC class I (MHC-I) molecules is the most selective even
6    Cross-presentation of phagocytosed Ags by MHC class I (MHC-I) molecules is thought to involve tran
7            Natural killer (NK) cells express MHC class I (MHC-I)-specific receptors, such as Ly49A, t
8 ciated with defect in trafficking of peptide-MHC class I (pMHC) complexes to the cell surface.
9                           Intratracheal anti-MHC class I Abs or hydrochloric acid in Foxp3-DTR mice i
10           Intratracheal instillation of anti-MHC class I Abs, but not isotype control, followed by mu
11  of defective ribosomal products relevant to MHC class I Ag presentation, we engineered influenza A v
12 ei GAP5040-48 epitope in mice expressing the MHC class I allele H-2D(b).
13            Thirty-five previously unreported MHC class I alleles are described.
14 ing RT-PCR from blood, we examined expressed MHC class I alleles from 38 wild mallards (Anas platyrhy
15                          For those orangutan MHC class I allotypes that are detected by human monoclo
16 mediators of antigen presentation, including MHC class I and beta2 microglobulin, were highly suscept
17 and exhibit enhanced activity of the classic MHC class I and class II antigen-presentation pathways.
18 ivated CD4 and CD8 genes in mice with intact MHC class I and class II molecules with the hypothesis t
19 ed from endogenous and exogenous sources for MHC class I and class II molecules, respectively.
20 o result in peptide binding strongly to both MHC class I and class II molecules, with matched HLA typ
21 RPalpha(+)) and CD8alpha(+) readily acquired MHC class I and II from thymic epithelial cells but plas
22 , we investigated the molecular evolution of MHC class I and II genes in five closely related species
23 ses and MHC-like chaperones that support the MHC class I and II molecules in presenting peptides to t
24 ike protein antigens, which are presented on MHC class I and II molecules, lipids can only be present
25        Polymorphonuclear cell Ecto expressed MHC class I and inhibited NK cell function.
26 an illustrated review of the ins and outs of MHC class I and MHC class II antigen presentation.
27 entified 4 influenza- and 3 allergen-derived MHC class I and MHC class II candidate T-cell epitopes w
28                            Furthermore, both MHC class I and MHC class II expression was upregulated
29 years to arrive at a coherent picture of how MHC class I and MHC class II molecules really work.
30 een proposed to perform specialized roles in MHC class I antigen presentation, cytokine modulation, a
31 croglobulin (B2M), an essential component of MHC class I antigen presentation, in 29.4% of patients w
32 -antigen load, but is highly correlated with MHC class I antigen presenting machinery expression (APM
33 atypical ubiquitination in the modulation of MHC class I antigen processing.
34                           Alterations of the MHC class I antigen-processing and presentation machiner
35                            The processing of MHC class I antigenic precursor peptides by the endoplas
36 e of the ERAP-mediated processing pathway of MHC class I antigens.
37 t lactational transfer of immunity can cross MHC class I barriers and that Th1 immunity can be impart
38 edge, of a broader repertoire of alternative MHC class I binders.
39 8alphaalpha on this cell used rat nonclassic MHC class I C/E16 on the target T cells as a ligand to i
40 s with elevated expression of rat nonclassic MHC class I C/E16 were highly susceptible to the killing
41 conventional MHC encoded class I gene, MICA (MHC class I chain-related gene A).
42                                              MHC class I chain-related proteins A and B (MICA and MIC
43 s demonstrated that expression of the common MHC class I component beta2-microglobulin (beta2M) by ca
44 between DNAM-1 and NKG2A that occurs even in MHC class I deficient mice.
45                  In this article, we examine MHC class I diversity in wild mallard ducks, the natural
46                                              MHC class I downregulation represents a significant chal
47 ng KIR or Ly49 receptors that recognize self-MHC class I during immune response to viral infections i
48 matic mutations is associated with defective MHC class I expression, impaired cytotoxic T cell activa
49 RNPR acts as a general positive regulator of MHC class I expression.
50 ws combinatorial fine-tuning of the level of MHC class I gene expression in response to intrinsic and
51 ents-CCAAT, TATAA-like, Sp1BS, and Inr-of an MHC class I gene in primary B-cells during both basal an
52                  An in-depth analysis of the MHC class I gene repertoire in the two orangutan species
53                                   Three duck MHC class I genes (UBA, UCA, and UEA) are predicted to b
54                  Strikingly, nearby tap2 and MHC class I genes also retain ancient sequence lineages,
55 ed MHC class I, UAA, although they have five MHC class I genes in the complex, arranged TAP1-TAP2-UAA
56               We show that expression of the MHC class I genes is downregulated in HPV-positive kerat
57 tic ducks predominantly use UAA, one of five MHC class I genes, but whether biased expression is also
58 ng 5], is a key transcription coactivator of MHC class I genes.
59                                      Loss of MHC class I has been described as a major immune evasion
60 ing EV biogenesis, no obvious editing of the MHC class I immunopeptidome occurs.
61                                 However, the MHC class I immunopeptidome of EVs has not been establis
62                          The notion that the MHC class I immunopeptidome presents only a small fracti
63 y a dramatic upregulation of CD83, CD86, and MHC class I in response to TLR3 and TLR7/8-agonists.
64                                              MHC class I is critically involved in defense against vi
65 first study to identify endogenous and viral MHC class I ligands for any bat species and, as such, pr
66          Thus, activating receptors for self-MHC class I modulate the differentiation of MCMV-specifi
67                   Individuals expressing the MHC class I molecule HLA-A2 produce cytotoxic T lymphocy
68 the macaque A2*05 gene encodes a specialized MHC class I molecule, and is most likely transported to
69 ctrometry approach to demonstrate that a bat MHC class I molecule, Ptal-N*01:01, binds antigenic pept
70 oded E3-19K immunomodulatory protein targets MHC class I molecules for retention within the endoplasm
71                                              MHC class I molecules have crucial roles in antigen pres
72 by their sensitivity to inhibition by "self" MHC class I molecules in a process called "education." I
73 r cells by recognizing peptides presented by MHC class I molecules on the cell surface.
74 nic MLR; however, they express low levels of MHC class I molecules that can efficiently acquire antig
75  optimisation by promoting peptide-receptive MHC class I molecules to associate with the peptide-load
76 peptides derived from endogenous proteins on MHC class I molecules to be recognized and targeted for
77         The cell surface expression level of MHC class I molecules varies as much as 10-fold between
78  TAP2 and reduce levels of the TAP1 subunit, MHC class I molecules, and EBNA1, a protein expressed in
79 ilities the reglucosylation of the glycan on MHC class I molecules, promoting their recognition by ca
80 d monitored the effects on the biogenesis of MHC class I molecules, the solubility of mutant forms of
81 redirect human polyclonal Tregs toward donor-MHC class I molecules, which are ubiquitously expressed
82 tion processes controlling the expression of MHC class I molecules, with a particular focus on their
83 e association of UGT1 with peptide-receptive MHC class I molecules.
84 s important for optimal peptide selection by MHC class I molecules.
85 c reticulum-associated degradation (ERAD) of MHC class I molecules.
86 ed on recognizing oligopeptides presented by MHC class I molecules.
87 shared tumor antigens in the context of host MHC class I molecules.
88 tive regulator of classical and nonclassical MHC class I molecules.
89 to peptides presented on the cell surface by MHC class I molecules.
90            We demonstrated that HNRNPR binds MHC class I mRNAs in their 3' untranslated regions and e
91 ulation, IFNgamma production, and killing of MHC class I negative hematopoietic grafts.
92                               Elimination of MHC class I on CD301b(+) dendritic cells abrogates prote
93 AT prime-boost vaccinations targeting either MHC class I or II neoantigens or tumor-associated antige
94                         Disruption of either MHC class I or LILRB1 potentiated phagocytosis of tumor
95 ies that fit very poorly to the conventional MHC class I pathway and suggest they are presented via a
96 l of the recognition of HIV infection by the MHC class I pathway.
97 the first time, establish EVs as a source of MHC class I peptides that can be used for the study of t
98                                Fast-evolving MHC class I polymorphism serves to diversify NK cell and
99 ncoding CPXV12 and CPXV203 to prevent direct MHC class I presentation of viral peptides by infected c
100 sulfite sequencing and show that none of the MHC class I promoters are inactivated by methylation.
101 that unrealized structural flexibility makes MHC class I receptive to parasite-derived ligands that e
102 tory receptors that are responsible for self-MHC class I recognition; beyond their inhibitory functio
103            Vitiligo risk associated with the MHC class I region thus derives from combined quantitati
104 f spliced peptides in the composition of the MHC class I repertoire.
105                                              MHC class I tetramers were assembled and binding cells w
106  how E3-19K proteins selectively engage with MHC class I to abrogate Ag presentation and counteract a
107                                              MHC class I transactivator (CITA), NLRC5 [nucleotide-bin
108 icroRNA, whereas the predominantly expressed MHC class I UAA is not.
109  on mouse and human beta-cells by inhibiting MHC class I upregulation.
110 he strength of balancing selection acting on MHC class I versus class II genes.
111 are internalized, degraded, and presented by MHC class I, is crucial to prime CD8 T cell responses.
112 led to rescue Nef-induced down-regulation of MHC class I, suggesting a possible mechanism for attacki
113  known to interact with peptide in mammalian MHC class I, suggesting the diversity is functional.
114 ynchos, there is one predominantly expressed MHC class I, UAA, although they have five MHC class I ge
115 to Ag-loaded exosomes were dependent on host MHC class I, with a critical role for splenic langerin(+
116                                              MHC class I-associated peptides (MAPs) define the immune
117 e of the JCI, Pearson et al. describe 25,270 MHC class I-associated peptides presented by a wide rang
118 -independent pathways robustly contribute to MHC class I-based immunosurveillance.
119                    We identified several bat MHC class I-binding partners, including calnexin, calret
120 was associated with reduced capacity to kill MHC class I-deficient hematopoietic grafts.
121 numbers of peripheral NK cells, clearance of MHC class I-deficient tumors in vivo, and cytotoxicity a
122 ion at particular developmental stages in an MHC class I-dependent manner.
123 ll specificity depends on the recognition of MHC class I-epitope complexes at the cell surface.
124         Although the MCMV genome encodes for MHC class I-homologous decoy ligands for inhibitory NK c
125 d they recognize glycolipids presented by an MHC class I-like CD1d molecule.
126 both in vitro and in vivo, which defines the MHC class I-LILRB1 signaling axis as an important regula
127 of immunity to Mycobacterium tuberculosis in MHC class I-mismatched animals, as well as from Th1-bias
128 geting cancer cells with intact and impaired MHC class I-related APM.
129                      Their ligands, that is, MHC class I-related chain (MIC) A/B and UL16-binding pro
130         A critical role was demonstrated for MHC class I-related chain A and B and membrane-bound IL-
131                                              MHC class I-related molecule MR1 presents riboflavin- an
132 e that the requirement for ubiquitylation in MHC class I-restricted Ag processing varies with class I
133 tional as judged by IFN-gamma production and MHC class I-restricted cytotoxicity.
134 MV-based vaccine vectors expressing a single MHC class I-restricted high-avidity epitope provided str
135  NKT cell-activating glycolipid linked to an MHC class I-restricted peptide from a viral antigen in h
136                                The supply of MHC class I-restricted peptides is primarily ensured by
137                                              MHC class I-restricted spliced epitopes have been descri
138 s-present cell corpse-associated antigens to MHC class I-restricted T cells, a property that was asso
139  antigens associated with apoptotic cells to MHC class I-restricted T cells.
140 hout compromising cell surface expression of MHC class I.
141 both inhibitory and activating receptors for MHC class I.
142  human cell line K562, which is deficient in MHC class I/II and CD1 expression, we generated an aAPC
143 ation and promotes a sustained expression of MHC class I/peptide complexes in the cell surface of DCs
144 esented by major histocompatibility complex (MHC) class I and class II molecules.
145 ibition of major histocompatibility complex (MHC) class I and class II.
146 l role for major histocompatibility complex (MHC) class I in controlling the phagocytic function of m
147 or presentation by major histocompatibility (MHC) class I molecules (pMHCs I) on the cell surface.
148 esented on major histocompatibility complex (MHC) class I molecules in an autophagy-dependent fashion
149 surface by major histocompatibility complex (MHC) class I molecules.
150 ntation by major histocompatibility complex (MHC) class I proteins initiates CD8(+) T cell-mediated i
151 tricted by major histocompatibility complex (MHC) class I, although rare examples of MHC class II res
152 ted by the major histocompatibility complex (MHC) class I-like molecule, CD1d.
153 to improve major histocompatibility complex (MHC) class I-mediated antigen presentation for the resol
154 he role of major histocompatibility complex (MHC) class I-related chain A (MICA) in BKPyV reactivatio
155 ted by the major histocompatibility complex (MHC) class I-related molecule MR1.
156 hat encode major histocompatibility complex (MHC) class I-restricted T-cell receptors (TCRs) or chime
157                             We observed that MHC-class I acquisition by recipient DCs occurs for at l
158 , we focused on the contribution of acquired MHC-class I on recipient DCs during the life span of a s
159                        In addition, acquired MHC-class I:peptide complexes stimulate T cell responses
160 mination by a human, preproinsulin reactive, MHC class-I-restricted CD8+ T cell clone (1E6) that can
161        The major-histocompatibility-complex-(MHC)-class-I-related molecule MR1 can present activating
162 lecule that predominantly binds and presents MHC class Ia leader sequence-derived peptides for NK cel
163 cules as well as the essentially monomorphic MHC class Ib (MHC-Ib) molecules.
164 that respond to glycolipids presented by the MHC class Ib molecule CD1d and are rapidly activated to
165     MHC-E is a highly conserved nonclassical MHC class Ib molecule that predominantly binds and prese
166  cells selected from a single mouse or human MHC class II (MHC II) in mice containing the human TCR g
167 transgenic mice expressing the MS-associated MHC class II (MHC-II) gene, HLA-DR2a, and T-cell recepto
168                                              MHC class II (MHC-II) molecules are critical in the cont
169 vaccines encoding proteins that target Ag to MHC class II (MHC-II) molecules on APCs have been shown
170 rface of antigen presenting cells (APCs) via MHC class II (MHC-II) molecules.
171              However, alternative sources of MHC class II (MHC-II)-restricted Ags have been described
172            The development and activation of MHC class II (MHC-II)-restricted CD4(+) T cells are dist
173 ly control of Brucella in the lungs, whereas MHC class II (MHCII) and IFN-gammaR deficiency impairs l
174 tolerogenic phenotype by diminishing surface MHC class II (MHCII) and promoting the tolerogenic marke
175 in (CD74) mediates assembly and targeting of MHC class II (MHCII) complexes.
176 tion of hundreds of peptides bound to murine MHC class II (MHCII) molecules.
177 tophagy (CMA), which promotes Ag capture and MHC class II (MHCII) presentation in B cells and signali
178 epithelial cell (mTEC) lineage from immature MHC class II (MHCII)(lo) to mature MHCII(hi) mTECs has r
179 on and reduction of surface-localized mature MHC class II (mMHCII).
180 tion by CD4 T cell responses by manipulating MHC class II Ag presentation and CD4 T cell activation a
181 rcellular Ag transfer, followed by classical MHC class II Ag processing via endocytosis, sensitized n
182 al autoimmune encephalomyelitis severity was MHC class II allele dependent, because the lack of TSSP
183                         Here, we defined the MHC class II alleles for immunodominant Gag CD4(+) T cel
184 itopes in CFP-10 were characterized, and the MHC class II alleles restricting them were determined.
185 th features that allow them to bind multiple MHC class II alleles.
186 cetylcholine receptor (AChR) response in MG, MHC class II and alpha-AChR subunit as well as chemokine
187 (-) cDC, expressing higher levels of CD172a, MHC class II and CD11b.
188 ticle, we show that their emergence required MHC class II and CD40/CD40L interactions.
189 appabeta, resulting in a sharp inhibition of MHC class II and costimulatory molecules (CD40, CD86) ex
190           These defects in the expression of MHC class II and costimulatory molecules corresponded wi
191  Ara h 1 that display promiscuous binding to MHC class II and induce TH2 cytokine production by T cel
192 cted, WT mice expressed significantly higher MHC class II and the co-stimulatory molecule CD80 compar
193 c forms and cysts, reduced the expression of MHC class II and the costimulatory molecule CD40 on the
194            This process is sensitive to anti-MHC class II antibodies.
195 therin in vivo to improved DC activation and MHC class II antigen presentation.
196 eview of the ins and outs of MHC class I and MHC class II antigen presentation.
197  early endosomes and proper sorting into the MHC class II antigen-presenting compartment (MIIC).
198 dentified by using in silico predictions and MHC class II binding assays.
199                                    In silico MHC class II binding prediction was performed with NetMH
200 enza- and 3 allergen-derived MHC class I and MHC class II candidate T-cell epitopes with potential an
201 4 T cell repertoire, features of TcR-peptide:MHC class II complex have a strong deterministic influen
202     We found that, despite having equivalent MHC class II expression and in vitro survival, moDCs wer
203 tiated into CD11c(+) cells in vivo with high MHC class II expression and induced decreased tumor burd
204 rences in infection status, cell lineage and MHC class II expression by antigen-bearing cells correla
205 HDM sensitization was performed in mice with MHC class II expression restricted to the B-cell lineage
206 contrast, HDM sensitization of mice in which MHC class II expression was restricted to B cells reveal
207            Furthermore, both MHC class I and MHC class II expression was upregulated at the hepatocel
208 pal component analysis, we found that robust MHC class II expression, coupled with appropriate costim
209 ajor functional cluster genes, including the MHC class II family, cytokines, chemokines, and co-stimu
210 dhesion complex genes, and were depleted for MHC class II genes.
211                   Here, we fine-map vitiligo MHC class II genetic risk to three SNPs only 47 bp apart
212  sclerosis (MS) is most strongly conveyed by MHC class II haplotypes, possibly by shaping the autoimm
213 fy the risk factors for MS conferred by some MHC class II haplotypes.
214 n (IL)-2, but not IL-17A; iii) high-affinity MHC class II interaction with SAgs, but not MHC-related
215  and traffics rapidly but transiently to the MHC class II loading compartment, as does Ag conjugated
216 ulsed MoDC, the duration of KLH residence in MHC class II loading compartments was significantly redu
217 trains migration of skin and BMDCs, supports MHC class II maturation, and promotes stable interaction
218 ose selected by a non-autoimmunity-promoting MHC class II molecule I-A(b).
219 t of a monoclonal antibody against the donor MHC class II molecule I-A(k) conjugated with the plant-d
220 ons with Ag receptors specific for a foreign MHC class II molecule type loaded with peptides from leu
221  investigated how NY-ESO-1 is processed onto MHC class II molecules for direct CD4(+) T cell recognit
222 T cells that recognize peptides presented by MHC class II molecules have been observed in a macaque S
223 at a coherent picture of how MHC class I and MHC class II molecules really work.
224                                Using peptide-MHC class II molecules to identify Cryptococcus-specific
225 t superantigens more efficiently than murine MHC class II molecules, CD4 CD8 double knockout (DKO) mi
226 tion markers, that is, CD40, CD80, CD86, and MHC class II molecules.
227 ne-capture assays, and staining with peptide:MHC class II multimers, all of these have significant te
228 gulation of costimulatory molecules CD86 and MHC class II on moDCs induced by B cells.
229 ntially including cross-presentation via the MHC class II pathway.
230 rth American population and with an in vitro MHC class II peptide reporter assay performed in paralle
231              Donor DC-restricted deletion of MHC class II phenocopied this Treg deficiency and cGVHD.
232 acroautophagy targeting of NY-ESO-1 enhanced MHC class II presentation.
233 phagy-dependent endogenous Ag processing for MHC class II presentation.
234                         In comparison to the MHC class II region in other mammals, the corresponding
235 non-LS defined by 17 variants located in the MHC class II region was found.
236 68 non-LS-associated variants located in the MHC class II region were identified and confirmed.
237 rst long-read sequence assembly of the horse MHC class II region with rigorous manual gene annotation
238 l Chromosome (BAC) clones spanning the horse MHC class II region.
239 une vitiligo is strongly associated with the MHC class II region.
240 eded for the regulatory T cell (Treg) arm of MHC class II responses.
241  supports both helper and regulatory arms of MHC class II responses.
242 lex (MHC) class I, although rare examples of MHC class II restriction have been reported in Cd4-defic
243                                 We performed MHC class II tetramer analyses, assays to detect intrace
244                                              MHC class II tetramer binding revealed a broad HLA-DR cr
245           Unlike effector CD4(+) T cells, an MHC class II tetramer reagent specific for T. gondii did
246 teins VP1 and VP2 were identified by peptide/MHC class II tetramer-guided epitope mapping, validated
247 observed significantly higher frequencies of MHC class II tetramer-positive CD4(+) T cells in HIV con
248                            Here, we employed MHC class II tetramers designed to immunodominant Gag ep
249 opes in clade C virus infection, constructed MHC class II tetramers, and then used these to define th
250 was positive for maternal immunogen-specific MHC class II tetramers.
251 etermined by utilizing ex vivo staining with MHC class II tetramers.
252  were screened using M.tuberculosis-specific MHC class II tetramers.
253 onversion has maintained higher diversity of MHC class II than class I in prairie grouse.
254  a stronger role in shaping the evolution of MHC class II than class I.
255 eam of defective antigen presentation within MHC class II that is induced by aGVHD.
256 CD25), CD27, CXCR3, DPP4 (CD26), GPR183, and MHC class II transcripts and proteins.
257                   Thus, this CD8alphaalpha(+)MHC class II(+) cell was a dually functional Ag-presenti
258         We have identified a CD8alphaalpha(+)MHC class II(+) cell with professional APC capacity duri
259 ia both tip and lateral routes, tip-resident MHC class II(+) cells are located significantly closer t
260  by inducing the expression of human HO-1 in MHC class II(+) cells in transgenic mice.
261 a substantial percentage of which were CD4(+)MHC class II(+), accumulated in the pup thymus and splee
262 ion in estrogen transduction pathway altered MHC Class II, alpha-AChR, and CXCL13 expression.
263 nses to infected B cells by targeting IL-12, MHC class II, and lysosomal proteases.
264 liferating CD B cells express high levels of MHC class II, CD80, and CD86.
265     Furthermore, they have low expression of MHC class II, costimulatory molecules, and low arginase1
266 l divisions from C57BL/6 donors but not from MHC class II- or CD40-deficient donors.
267 lopment of transplant arteriosclerosis in an MHC class II-mismatched allograft model.
268 jection of major antigen-mismatched skin and MHC class II-mismatched cardiac allografts.
269 fic Th2 cells for the treatment of mice with MHC class II-negative myeloma.
270 s from infected mice and ovalbumin-specific, MHC class II-restricted alpha/beta (OT-II) T cells refle
271 genetic loci of M. tuberculosis that inhibit MHC class II-restricted antigen presentation by mycobact
272 vivo, and a PE_PGRS47 mutant showed enhanced MHC class II-restricted antigen presentation during in v
273 hat are genetically engineered to express an MHC class II-restricted antitumor TCR that targets MAGE-
274 y autoreactive CD4(+) T cells in response to MHC class II-restricted autoantigen activation by 33D1(+
275  of CD4(+) T cells and a large population of MHC class II-restricted CD8alphaalpha T cells that are g
276 fector subsets, including ThCTL that mediate MHC class II-restricted cytotoxicity.
277 f an adoptive CD4(+) T-cell therapy using an MHC class II-restricted, HLA-DPB1*0401-restricted TCR th
278 gE complex uptake by B cells directed Ags to MHC class II-rich compartments.
279                                  Blockade of MHC class II-TCR interaction led to selective expansion
280 TLA-4 interaction with CD80/CD86, as well as MHC class II-TCR interaction within mouse Treg pools and
281 ivation and maturation, i.e. CD40, CD86, and MHC class II.
282  region were almost exclusively presented by MHC class II.
283 upregulation of LPS-induced CD80, CD274, and MHC class II.
284  a manner similar to that observed with anti-MHC class II.
285 sponses and the epitope preferentially binds MHC class II/IA(k) rather than IE(k) By creating IA(k)/a
286 ression of major histocompatibility complex (MHC) class II antigen presentation is believed to be amo
287  predicted major histocompatibility complex (MHC) class II binding peptides.
288 ted by the major histocompatibility complex (MHC) class II molecule I-A(g7) (associated with the deve
289 ading onto major histocompatibility complex (MHC) class II molecules.
290 ion within major histocompatibility complex (MHC) class II of donor dendritic cells (DCs) is markedly
291  Recently, major histocompatibility complex (MHC) class II tetramers have emerged as a powerful tool
292 coding the major histocompatibility complex (MHC) class II transactivator, CIITA.
293    Because major histocompatibility complex (MHC) class II(+) cells are most efficient at inducing im
294 a panel of major histocompatibility complex (MHC) class II-matched CD4(+)T cells and found that LANA-
295 cells, and major histocompatibility complex (MHC) class II-positive antigen-presenting cells (APCs) b
296  generated major histocompatibility complex (MHC) class II-restricted T cell hybridomas from IKEPLUS-
297 lesions, recognized distinct non-overlapping MHC-class-II-restricted peptides derived from the same p
298          Here, we characterized the genes of MHC class IIB chain of the Midas cichlid species complex
299 d has one of the most diverse repertoires of MHC class IIB genes known, which could serve as a powerf
300 cally rare major histocompatibility complex (MHC) class IIb genotypes were infected by fewer parasite
301 we analyzed a new genetic association in the MHC class-III region (MHC-III) using adjuvant- and antig

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