Ignet

Gene Information

Gene symbol: HLA-C

Gene name: major histocompatibility complex, class I, C

HGNC ID: 4933

Related Genes

#	Gene Symbol	Number of hits
1	CD8A	1 hits
2	HCP5	1 hits
3	HLA-A	1 hits
4	HLA-B	1 hits
5	HLA-DOB	1 hits
6	HLA-DQA1	1 hits
7	HLA-DQB1	1 hits
8	HLA-DRA	1 hits
9	HLA-DRB1	1 hits
10	HLA-DRB5	1 hits
11	HLA-G	1 hits
12	HLA-H	1 hits
13	IFNG	1 hits
14	IL15	1 hits
15	KIR2DL1	1 hits
16	KIR2DL2	1 hits
17	KIR3DL1	1 hits
18	MAGEA12	1 hits
19	MLANA	1 hits
20	PSMB9	1 hits
21	S100B	1 hits
22	TAP1	1 hits
23	TAP2	1 hits
24	ZNRD1	1 hits

Related Sentences

#	PMID	Sentence
1	9816214	Specific CD8(+) CTL recognition of melanoma requires expression of MHC class I molecules as well as melanoma-associated peptide epitopes.
2	9816214	Stable MHC class I cell surface expression requires delivery of cytosolic peptides into the endoplasmic reticulum by the peptide transporter molecules TAP1 and TAP2, with peptides subsequently transported to the cell surface in complexes containing MHC class I heavy chain and beta2-microglobulin.
3	9816214	We have evaluated a series of mechanisms resulting in MHC class I down-regulation in a human melanoma cell line, Mz18, typed as HLA-A2(+), A3(+), B7(+), B57(+), Cw1(+), and Cw6(+) by genomic PCR analysis.
4	9816214	The melanoma cell line Mz18 exhibits a global down-regulation of MHC class I heavy chain transcripts; beta2-microglobulin; the proteasome subunits LMP2/7, involved in generating cytosolic peptide fragments; and the peptide transporter molecules TAP1 and TAP2, involved in peptide transport from the cytosol into the endoplasmic reticulum.
5	9816214	IFN-gamma treatment of Mz18 melanoma cells leads to up-regulation of LMP2/7 and TAP1/2, as well as to up-regulation of HLA-B and HLA-C MHC loci alleles, but not HLA-A2 or HLA-A3.
6	9816214	Melanoma peptides could only be presented and recognized by CTLs if the HLA-A2-transfected Mz18 cell line was first treated with IFN-gamma, thereby restoring LMP2/7 and TAP1/2 expression and function.
7	9816214	Because several melanoma antigens recognized by T cells have been reported to be presented by HLA-A2 (MART-1/Melan-A, tyrosinase, gp100, and MAGE-3), the loss of HLA-A2 molecules may represent an important mechanism by which many melanomas evade immune recognition.
8	9816214	These findings suggest that patients entering clinical trials for immunotherapy with melanoma vaccines should be carefully examined for tumor cell allelic MHC class I loss and whether such MHC class I antigen down-regulation can be restored by cytokines.
9	11182225	We identified 4 HLA-A, 7 HLA-B, and 5 HLA-C specificities that were observed at high frequencies in the Botswana population: A30, A02, A23, A68, B58, B72, B42, B8, B18, B44, B45, Cw7, Cw2, Cw17, Cw6, and Cw4.
10	12673681	Clinical and immunological evaluation of patients with metastatic melanoma undergoing immunization with the HLA-Cw*0702-associated epitope MAGE-A12:170-178.
11	12673681	Patients with metastatic melanoma who expressed HLA-Cw*0702 and whose tumors had demonstrable MAGE-A12 expression were immunized with the peptide MAGE-A12:170-178 administered subcutaneously in incomplete Freund's adjuvant (IFA).
12	12673681	Nine patients were selected for vaccination based on MAGE-A12 expression and the presence of HLA-Cw*0702.
13	12673681	The immune response was monitored both by tetrameric HLA-Cw*0702/MAGE-A12:170-178 complexes and by analysis of interferon-gamma mRNA transcription using a quantitative real-time polymerase chain reaction assay after peptide-specific stimulation.
14	12673681	Clinical and immunological evaluation of patients with metastatic melanoma undergoing immunization with the HLA-Cw*0702-associated epitope MAGE-A12:170-178.
15	12673681	Patients with metastatic melanoma who expressed HLA-Cw*0702 and whose tumors had demonstrable MAGE-A12 expression were immunized with the peptide MAGE-A12:170-178 administered subcutaneously in incomplete Freund's adjuvant (IFA).
16	12673681	Nine patients were selected for vaccination based on MAGE-A12 expression and the presence of HLA-Cw*0702.
17	12673681	The immune response was monitored both by tetrameric HLA-Cw*0702/MAGE-A12:170-178 complexes and by analysis of interferon-gamma mRNA transcription using a quantitative real-time polymerase chain reaction assay after peptide-specific stimulation.
18	12673681	Clinical and immunological evaluation of patients with metastatic melanoma undergoing immunization with the HLA-Cw*0702-associated epitope MAGE-A12:170-178.
19	12673681	Patients with metastatic melanoma who expressed HLA-Cw*0702 and whose tumors had demonstrable MAGE-A12 expression were immunized with the peptide MAGE-A12:170-178 administered subcutaneously in incomplete Freund's adjuvant (IFA).
20	12673681	Nine patients were selected for vaccination based on MAGE-A12 expression and the presence of HLA-Cw*0702.
21	12673681	The immune response was monitored both by tetrameric HLA-Cw*0702/MAGE-A12:170-178 complexes and by analysis of interferon-gamma mRNA transcription using a quantitative real-time polymerase chain reaction assay after peptide-specific stimulation.
22	12673681	Clinical and immunological evaluation of patients with metastatic melanoma undergoing immunization with the HLA-Cw*0702-associated epitope MAGE-A12:170-178.
23	12673681	Patients with metastatic melanoma who expressed HLA-Cw*0702 and whose tumors had demonstrable MAGE-A12 expression were immunized with the peptide MAGE-A12:170-178 administered subcutaneously in incomplete Freund's adjuvant (IFA).
24	12673681	Nine patients were selected for vaccination based on MAGE-A12 expression and the presence of HLA-Cw*0702.
25	12673681	The immune response was monitored both by tetrameric HLA-Cw*0702/MAGE-A12:170-178 complexes and by analysis of interferon-gamma mRNA transcription using a quantitative real-time polymerase chain reaction assay after peptide-specific stimulation.
26	15009803	The allelic and haplotypic diversity of the HLA-A, HLA-B, and HLA-C loci was investigated in 852 subjects from five sub-Saharan populations from Kenya (Nandi and Luo), Mali (Dogon), Uganda, and Zambia.
27	15009803	The strength of the LD associations between alleles of HLA-A and HLA-B loci and those of HLA-B and HLA-C loci was on average of the same or higher magnitude as those observed in other non-African populations for the same pairs of loci.
28	15009803	The allelic and haplotypic diversity of the HLA-A, HLA-B, and HLA-C loci was investigated in 852 subjects from five sub-Saharan populations from Kenya (Nandi and Luo), Mali (Dogon), Uganda, and Zambia.
29	15009803	The strength of the LD associations between alleles of HLA-A and HLA-B loci and those of HLA-B and HLA-C loci was on average of the same or higher magnitude as those observed in other non-African populations for the same pairs of loci.
30	15383595	Ten epitopic regions were identified across p17, p24, and p2p7p1p6, and greater than two-thirds of targeted regions were directed at: TGTEELRSLYNTVATLY (p17, 35%); GPKEPFRDYVDRFFKTLRAEQATQDV (p24, 19%); and RGGKLDKWEKIRLRPGGKKHYMLKHL (p17, 15%).
31	15383595	Fine epitope mapping revealed that five of nine identified optimal Gag epitopes were novel: HLVWASREL, LVWASRELERF, LYNTVATLY, PFRDYVDRFF, and TLRAEQATQD, and were restricted by unique HLA-Cw08, HLA-A30/B57, HLA-A29/B44, and HLA-Cw03 alleles, respectively.
32	15603879	Of all the alleles analyzed, HLA-B3503 (median SI, 3.00; p = 0.031) and HLA-Cw1502 (median SI, 3.19; p = 0.035) were positively associated with lymphoproliferative responses to rubella virus antigens, whereas the HLA-B*3901 (SI, 1.34; p = 0.066) allele was negatively associated.
33	15665097	The highly polymorphic gene products of the classical MHC class I genes in humans (HLA-A, HLA-B, and HLA-C) play a critical role in the immune defense against intracellular infections.
34	16331510	Immunologic significance of HLA class I genes in measles virus-specific IFN-gamma and IL-4 cytokine immune responses.
35	16331510	Median values for measles-specific interferon gamma (IFN-gamma) and interleukin-4 (IL-4) cytokines were 40.7 pg/ml [interquartile range (IQR) 8.1-176.7] and 9.7 pg/ml (IQR 2.8-24.3), respectively.
36	16331510	Class I HLA-A (0101 and 3101) and HLA-Cw (0303 and 0501) alleles were significantly associated with measles-virus-induced IFN-gamma secretion.
37	16331510	HLA-A3101 and Cw0303 were associated with a higher median IFN-gamma response, while A0101 and Cw0501 were associated with lower measles-specific IFN-gamma response.
38	16331510	We found limited associations between HLA class I gene polymorphisms and Th2-like (IL-4) immune responses after measles vaccination, indicating that HLA class I molecules may have a limited effect on measles-vaccine-induced IL-4 secretion.
39	16451198	We investigated the genetic diversity of HLA-A, HLA-B and HLA-C alleles in remote populations of Cameroon.
40	16451198	Subjects from seven small, isolated, indigenous populations (N = 274) in the rainforest of southern Cameroon were typed for HLA-A, HLA-B and HLA-C alleles using a polymerase chain reaction/sequence-specific oligonucleotide probe assay and sequence analysis.
41	16451198	Multiple alleles of the HLA-A (N = 28), HLA-B (N = 41) and HLA-C (N = 21) loci were identified, of which A2301[allele frequency (AF) = 12.8%], B5802 (AF = 10.9%) and Cw0401 (AF = 16.6%) were the most frequent individual alleles and A02 (AF = 19.0%), B58 (AF = 15.9%) and Cw07 (AF = 22.4%) the most common serologically defined groups of alleles.
42	16451198	Heterozygosity values of 0.89, 0.92 and 0.89 were determined for HLA-A, HLA-B and HLA-C, respectively.
43	16451198	We investigated the genetic diversity of HLA-A, HLA-B and HLA-C alleles in remote populations of Cameroon.
44	16451198	Subjects from seven small, isolated, indigenous populations (N = 274) in the rainforest of southern Cameroon were typed for HLA-A, HLA-B and HLA-C alleles using a polymerase chain reaction/sequence-specific oligonucleotide probe assay and sequence analysis.
45	16451198	Multiple alleles of the HLA-A (N = 28), HLA-B (N = 41) and HLA-C (N = 21) loci were identified, of which A2301[allele frequency (AF) = 12.8%], B5802 (AF = 10.9%) and Cw0401 (AF = 16.6%) were the most frequent individual alleles and A02 (AF = 19.0%), B58 (AF = 15.9%) and Cw07 (AF = 22.4%) the most common serologically defined groups of alleles.
46	16451198	Heterozygosity values of 0.89, 0.92 and 0.89 were determined for HLA-A, HLA-B and HLA-C, respectively.
47	16451198	We investigated the genetic diversity of HLA-A, HLA-B and HLA-C alleles in remote populations of Cameroon.
48	16451198	Subjects from seven small, isolated, indigenous populations (N = 274) in the rainforest of southern Cameroon were typed for HLA-A, HLA-B and HLA-C alleles using a polymerase chain reaction/sequence-specific oligonucleotide probe assay and sequence analysis.
49	16451198	Multiple alleles of the HLA-A (N = 28), HLA-B (N = 41) and HLA-C (N = 21) loci were identified, of which A2301[allele frequency (AF) = 12.8%], B5802 (AF = 10.9%) and Cw0401 (AF = 16.6%) were the most frequent individual alleles and A02 (AF = 19.0%), B58 (AF = 15.9%) and Cw07 (AF = 22.4%) the most common serologically defined groups of alleles.
50	16451198	Heterozygosity values of 0.89, 0.92 and 0.89 were determined for HLA-A, HLA-B and HLA-C, respectively.
51	16451198	We investigated the genetic diversity of HLA-A, HLA-B and HLA-C alleles in remote populations of Cameroon.
52	16451198	Subjects from seven small, isolated, indigenous populations (N = 274) in the rainforest of southern Cameroon were typed for HLA-A, HLA-B and HLA-C alleles using a polymerase chain reaction/sequence-specific oligonucleotide probe assay and sequence analysis.
53	16451198	Multiple alleles of the HLA-A (N = 28), HLA-B (N = 41) and HLA-C (N = 21) loci were identified, of which A2301[allele frequency (AF) = 12.8%], B5802 (AF = 10.9%) and Cw0401 (AF = 16.6%) were the most frequent individual alleles and A02 (AF = 19.0%), B58 (AF = 15.9%) and Cw07 (AF = 22.4%) the most common serologically defined groups of alleles.
54	16451198	Heterozygosity values of 0.89, 0.92 and 0.89 were determined for HLA-A, HLA-B and HLA-C, respectively.
55	16882705	However, HLA-C-restricted CTLs were unaffected by Nef, consistent with down-regulation of cell-surface HLA-A and -B but not HLA-C molecules.
56	16882705	Thus, CTLs vary dramatically in their susceptibility to Nef interference, suggesting differences in the relative importance of HLA-A- and HLA-B- versus HLA-C-restricted CTLs in vivo.
57	16882705	However, HLA-C-restricted CTLs were unaffected by Nef, consistent with down-regulation of cell-surface HLA-A and -B but not HLA-C molecules.
58	16882705	Thus, CTLs vary dramatically in their susceptibility to Nef interference, suggesting differences in the relative importance of HLA-A- and HLA-B- versus HLA-C-restricted CTLs in vivo.
59	17106278	We found 10 class I alleles present in more than 10% of the population: HLA-A02, HLA-A11, HLA-A24, HLA-B13, HLA-B15, HLA-B40, HLA-Cw03, HLA-Cw07, HLA-Cw01, and HLA-Cw06.
60	17106278	Several class II alleles were found at high frequency (>or=10%): HLA-DRB3, HLA-DRB4, HLA-DRB5, HLA-DRB10701, HLA-DRB11501, HLA-DRB10401, HLA-DRB10901, HLA-DRB11201, HLA-DQB10601, HLA-DQB10301, HLA-DQB10201, HLA-DQB10501, and HLA-DQB0303.
61	17106278	The HLA-B14 allele was only found in the HIV-1-seropositive group, and many 2-locus haplotypes were significantly overrepresented in this group: HLA-B14/Cw08, HLA-B51/Cw14, HLA-A02/B13, HLA-A31/Cw14, HLA-A02/Cw06, and the class II haplotype HLA-DRB11301/DQB1*0601.
62	17106278	Alleles significantly increased in the HIV-1-seronegative controls were HLA-B44, HLA-Cw04, and HLA-DRB1*1402.
63	17106278	Overrepresented 2-locus haplotypes in the control group were HLA-B44/Cw04, HLA-A31/Cw03, HLA-A03/Cw07, HLA-A11/B13, HLA-A11/B38, HLA-A24/B52, and HLA-A11/Cw01.
64	17106278	We found 10 class I alleles present in more than 10% of the population: HLA-A02, HLA-A11, HLA-A24, HLA-B13, HLA-B15, HLA-B40, HLA-Cw03, HLA-Cw07, HLA-Cw01, and HLA-Cw06.
65	17106278	Several class II alleles were found at high frequency (>or=10%): HLA-DRB3, HLA-DRB4, HLA-DRB5, HLA-DRB10701, HLA-DRB11501, HLA-DRB10401, HLA-DRB10901, HLA-DRB11201, HLA-DQB10601, HLA-DQB10301, HLA-DQB10201, HLA-DQB10501, and HLA-DQB0303.
66	17106278	The HLA-B14 allele was only found in the HIV-1-seropositive group, and many 2-locus haplotypes were significantly overrepresented in this group: HLA-B14/Cw08, HLA-B51/Cw14, HLA-A02/B13, HLA-A31/Cw14, HLA-A02/Cw06, and the class II haplotype HLA-DRB11301/DQB1*0601.
67	17106278	Alleles significantly increased in the HIV-1-seronegative controls were HLA-B44, HLA-Cw04, and HLA-DRB1*1402.
68	17106278	Overrepresented 2-locus haplotypes in the control group were HLA-B44/Cw04, HLA-A31/Cw03, HLA-A03/Cw07, HLA-A11/B13, HLA-A11/B38, HLA-A24/B52, and HLA-A11/Cw01.
69	17263647	HLA-B alleles were involved in more associations (50%) than alleles from either the HLA-A (27%) or HLA-C (24%) loci.
70	18097665	A HLA-Cw*0701 restricted Melan-A/MART1 epitope presented by melanoma tumor cells to CD8+ tumor infiltrating lymphocytes.
71	18097665	Melan-A/MART1 is a melanocytic differentiation antigen recognized on melanoma tumor cells by CD8+ and CD4+ T cells.
72	18097665	In this study, we describe a new epitope of this protein recognized in the context of HLA-Cw*0701 molecules by a CD8+ tumor infiltrating lymphocyte (TIL) clone.
73	18097665	This CD8+ TIL clone specifically recognized and killed a fraction of melanoma cells lines expressing Melan-A/MART1 and HLA-Cw*0701.
74	18097665	A HLA-Cw*0701 restricted Melan-A/MART1 epitope presented by melanoma tumor cells to CD8+ tumor infiltrating lymphocytes.
75	18097665	Melan-A/MART1 is a melanocytic differentiation antigen recognized on melanoma tumor cells by CD8+ and CD4+ T cells.
76	18097665	In this study, we describe a new epitope of this protein recognized in the context of HLA-Cw*0701 molecules by a CD8+ tumor infiltrating lymphocyte (TIL) clone.
77	18097665	This CD8+ TIL clone specifically recognized and killed a fraction of melanoma cells lines expressing Melan-A/MART1 and HLA-Cw*0701.
78	18097665	A HLA-Cw*0701 restricted Melan-A/MART1 epitope presented by melanoma tumor cells to CD8+ tumor infiltrating lymphocytes.
79	18097665	Melan-A/MART1 is a melanocytic differentiation antigen recognized on melanoma tumor cells by CD8+ and CD4+ T cells.
80	18097665	In this study, we describe a new epitope of this protein recognized in the context of HLA-Cw*0701 molecules by a CD8+ tumor infiltrating lymphocyte (TIL) clone.
81	18097665	This CD8+ TIL clone specifically recognized and killed a fraction of melanoma cells lines expressing Melan-A/MART1 and HLA-Cw*0701.
82	18434400	Significantly more HLA-B (chi(2); P = 3.59 x 10(-5)) and HLA-C (chi(2); P = 4.71 x 10(-6)) alleles were associated with amino acid changes than HLA-A, highlighting their importance in driving viral evolution.
83	18982067	HIV-1 disease-influencing effects associated with ZNRD1, HCP5 and HLA-C alleles are attributable mainly to either HLA-A10 or HLA-B*57 alleles.
84	18982067	A recent genome-wide association study (GWAS) suggested that polymorphisms in or around the genes HCP5, HLA-C and ZNRD1 confer restriction against HIV-1 viral replication or disease progression.
85	18982067	We also find that because of linkage disequilibrium (LD) patterns, the dominant viral load- and disease-influencing associations for the ZNRD1 or HLA-C and HCP5 alleles are apparent mainly when these alleles are present in HLA-A10- or HLA-B*57-containing haplotypes, respectively.
86	18982067	Furthermore, HCP5 and HLA-C alleles stratify B57-containing genotypes into those that associate with either striking disease retardation or progressive disease, providing one explanation for the long-standing conundrum of why some HLA-B57-carrying individuals are long-term non-progressors, whereas others exhibit progressive disease.
87	18982067	They specifically demonstrate that the influence of ZNRD1 alleles on disease progression rates are attributable to HLA-A10, help clarify the relationship between the HCP5, HLA-C and HLA-B57 alleles, and reaffirm a critical role of HLA-B57 alleles in HIV disease.
88	18982067	HIV-1 disease-influencing effects associated with ZNRD1, HCP5 and HLA-C alleles are attributable mainly to either HLA-A10 or HLA-B*57 alleles.
89	18982067	A recent genome-wide association study (GWAS) suggested that polymorphisms in or around the genes HCP5, HLA-C and ZNRD1 confer restriction against HIV-1 viral replication or disease progression.
90	18982067	We also find that because of linkage disequilibrium (LD) patterns, the dominant viral load- and disease-influencing associations for the ZNRD1 or HLA-C and HCP5 alleles are apparent mainly when these alleles are present in HLA-A10- or HLA-B*57-containing haplotypes, respectively.
91	18982067	Furthermore, HCP5 and HLA-C alleles stratify B57-containing genotypes into those that associate with either striking disease retardation or progressive disease, providing one explanation for the long-standing conundrum of why some HLA-B57-carrying individuals are long-term non-progressors, whereas others exhibit progressive disease.
92	18982067	They specifically demonstrate that the influence of ZNRD1 alleles on disease progression rates are attributable to HLA-A10, help clarify the relationship between the HCP5, HLA-C and HLA-B57 alleles, and reaffirm a critical role of HLA-B57 alleles in HIV disease.
93	18982067	HIV-1 disease-influencing effects associated with ZNRD1, HCP5 and HLA-C alleles are attributable mainly to either HLA-A10 or HLA-B*57 alleles.
94	18982067	A recent genome-wide association study (GWAS) suggested that polymorphisms in or around the genes HCP5, HLA-C and ZNRD1 confer restriction against HIV-1 viral replication or disease progression.
95	18982067	We also find that because of linkage disequilibrium (LD) patterns, the dominant viral load- and disease-influencing associations for the ZNRD1 or HLA-C and HCP5 alleles are apparent mainly when these alleles are present in HLA-A10- or HLA-B*57-containing haplotypes, respectively.
96	18982067	Furthermore, HCP5 and HLA-C alleles stratify B57-containing genotypes into those that associate with either striking disease retardation or progressive disease, providing one explanation for the long-standing conundrum of why some HLA-B57-carrying individuals are long-term non-progressors, whereas others exhibit progressive disease.
97	18982067	They specifically demonstrate that the influence of ZNRD1 alleles on disease progression rates are attributable to HLA-A10, help clarify the relationship between the HCP5, HLA-C and HLA-B57 alleles, and reaffirm a critical role of HLA-B57 alleles in HIV disease.
98	18982067	HIV-1 disease-influencing effects associated with ZNRD1, HCP5 and HLA-C alleles are attributable mainly to either HLA-A10 or HLA-B*57 alleles.
99	18982067	A recent genome-wide association study (GWAS) suggested that polymorphisms in or around the genes HCP5, HLA-C and ZNRD1 confer restriction against HIV-1 viral replication or disease progression.
100	18982067	We also find that because of linkage disequilibrium (LD) patterns, the dominant viral load- and disease-influencing associations for the ZNRD1 or HLA-C and HCP5 alleles are apparent mainly when these alleles are present in HLA-A10- or HLA-B*57-containing haplotypes, respectively.
101	18982067	Furthermore, HCP5 and HLA-C alleles stratify B57-containing genotypes into those that associate with either striking disease retardation or progressive disease, providing one explanation for the long-standing conundrum of why some HLA-B57-carrying individuals are long-term non-progressors, whereas others exhibit progressive disease.
102	18982067	They specifically demonstrate that the influence of ZNRD1 alleles on disease progression rates are attributable to HLA-A10, help clarify the relationship between the HCP5, HLA-C and HLA-B57 alleles, and reaffirm a critical role of HLA-B57 alleles in HIV disease.
103	18982067	HIV-1 disease-influencing effects associated with ZNRD1, HCP5 and HLA-C alleles are attributable mainly to either HLA-A10 or HLA-B*57 alleles.
104	18982067	A recent genome-wide association study (GWAS) suggested that polymorphisms in or around the genes HCP5, HLA-C and ZNRD1 confer restriction against HIV-1 viral replication or disease progression.
105	18982067	We also find that because of linkage disequilibrium (LD) patterns, the dominant viral load- and disease-influencing associations for the ZNRD1 or HLA-C and HCP5 alleles are apparent mainly when these alleles are present in HLA-A10- or HLA-B*57-containing haplotypes, respectively.
106	18982067	Furthermore, HCP5 and HLA-C alleles stratify B57-containing genotypes into those that associate with either striking disease retardation or progressive disease, providing one explanation for the long-standing conundrum of why some HLA-B57-carrying individuals are long-term non-progressors, whereas others exhibit progressive disease.
107	18982067	They specifically demonstrate that the influence of ZNRD1 alleles on disease progression rates are attributable to HLA-A10, help clarify the relationship between the HCP5, HLA-C and HLA-B57 alleles, and reaffirm a critical role of HLA-B57 alleles in HIV disease.
108	19617574	The ability of CD8(+) T cells to engage a diverse range of peptide-major histocompatibility complex (MHC) complexes can also lead to cross-recognition of self and nonself peptide-MHC complexes and thus directly contribute toward allograft rejection or autoimmunity.
109	19617574	Functional characterization of a human leukocyte antigen (HLA) Cw*0602-restricted cytomegalovirus-specific CD8(+) T-cell response revealed an unusual dual specificity toward a pp65 epitope and the alloantigen HLA DR4.
110	19617574	Furthermore, allostimulation of peripheral blood lymphocytes with HLA DRB0401-expressing cells rapidly expanded CD8(+) T cells, which recognized the pp65 epitope in the context of HLA Cw0602.
111	19617574	The ability of CD8(+) T cells to engage a diverse range of peptide-major histocompatibility complex (MHC) complexes can also lead to cross-recognition of self and nonself peptide-MHC complexes and thus directly contribute toward allograft rejection or autoimmunity.
112	19617574	Functional characterization of a human leukocyte antigen (HLA) Cw*0602-restricted cytomegalovirus-specific CD8(+) T-cell response revealed an unusual dual specificity toward a pp65 epitope and the alloantigen HLA DR4.
113	19617574	Furthermore, allostimulation of peripheral blood lymphocytes with HLA DRB0401-expressing cells rapidly expanded CD8(+) T cells, which recognized the pp65 epitope in the context of HLA Cw0602.
114	21076072	Antibodies and lentiviruses that specifically recognize a T cell epitope derived from HIV-1 Nef protein and presented by HLA-C.
115	21076072	In this study, we describe the development of a high-affinity human Ab that specifically interacts, at low pM concentrations, with a conserved viral T cell epitope derived from HIV-1 Nef protein and presented by HLA-C.
116	21076072	Engineering lentiviruses to display this Ab endowed them with the same specificity as the Ab, whereas coexpressing the Ab and Fas ligand enables the lentiviruses to kill specifically Nef-presenting cells.
117	21076072	Antibodies and lentiviruses that specifically recognize a T cell epitope derived from HIV-1 Nef protein and presented by HLA-C.
118	21076072	In this study, we describe the development of a high-affinity human Ab that specifically interacts, at low pM concentrations, with a conserved viral T cell epitope derived from HIV-1 Nef protein and presented by HLA-C.
119	21076072	Engineering lentiviruses to display this Ab endowed them with the same specificity as the Ab, whereas coexpressing the Ab and Fas ligand enables the lentiviruses to kill specifically Nef-presenting cells.
120	21887282	A novel immunodominant CD8+ T cell response restricted by a common HLA-C allele targets a conserved region of Gag HIV-1 clade CRF01_AE infected Thais.
121	22074999	Human leukocyte antigen class I (A, B, C) and II (DRB1) diversity in the black and Caucasian South African population.
122	22074999	A cross-section of black and Caucasian South Africans (N = 302) were genotyped at high resolution (class I HLA-A, -B, -C and class II HLA-DRB1).
123	22074999	HLA-B, and HLA-C loci showed the strongest overall linkage disequilibrium (LD) and HLA-B/HLA-C two locus haplotypes also showed the strongest LD (D'(ij)) in both population groups.
124	22074999	HLA-A Supertype family phenotypic frequencies did not differ between the two populations, but four (B08, B27, B58, and B62) HLA-B Supertype families differed significantly.
125	23105270	The ARMS-PCR technology has been found to be particularly useful for typing HLA-A, HLA-B and HLA-Cw alleles.
126	23776170	HLA-A01:03, HLA-A24:02, HLA-B08:01, HLA-B27:05, HLA-B35:01, HLA-B44:02, and HLA-C*07:01 monochain transgenic/H-2 class I null mice: novel versatile preclinical models of human T cell responses.
127	23776170	In combination with the previously created HLA-A02:01 and -B07:02 transgenic mice, the novel HLA transgenic mice described in this report should be a versatile preclinical animal model that will speed up the identification and optimization of HLA-restricted CD8(+) T cell epitopes of potential interest in various autoimmune human diseases and in preclinical evaluation of T cell-based vaccines.
128	24012585	However, homozygosity at HLA-A, HLA-B or HLA-C conferred no observable disadvantage in our study population (P = 0.730, 0.246 and 0.445, respectively).
129	24075919	These SNPs were found to regulate the expression of a group of genes involved in antigen processing and presentation including HLA-A, HLA-C, HLA-G, HLA-H, HLA-DRA, HLA-DRB1, HLA-DRB5, HLA-DQA1, HLA-DQB1, HLA-DOB, and TAP-2.
130	24248811	Association and differentiation of MHC class I and II polymorphic Alu insertions and HLA-A, -B, -C and -DRB1 alleles in the Chinese Han population.
131	24248811	In order to investigate the polymorphism of Alu insertions (POALINs) in the HLA region, we genotyped ten Alu loci (AluMICB, AluTF, AluHJ, AluHG, AluHF in the HLA class I region and AluDPB2, AluDQA2, AluDQA1, AluDRB1, AluORF10 in the HLA class II region) to determine their allele frequencies and associations with the HLA-A, HLA-B, HLA-C and HLA-DRB1 genes in the Chinese Han population.
132	24248811	Each POALIN was in significant linkage disequilibrium with a variety of HLA-A, -B, -C and -DRB1 alleles, and was associated with a variety of HLA-A, -B, -C and -DRB1 allele in Chinese Han.
133	24798939	Associations of HLA-A, HLA-B and HLA-C alleles frequency with prevalence of herpes simplex virus infections and diseases across global populations: implication for the development of an universal CD8+ T-cell epitope-based vaccine.
134	24798939	The present report: (i) analyzes the prevalence of HSV-1 and HSV-2 infections across various regions of the world; (ii) analyzes potential associations of common HLA-A, HLA-B and HLA-C alleles with the prevalence of HSV-1 and HSV-2 infections in the Caucasoid, Oriental, Hispanic and Black major populations; and (iii) discusses how our recently developed HLA-A, HLA-B, and HLA-C transgenic/H-2 class I null mice will help validate HLA/herpes prevalence associations.
135	24798939	Overall, high prevalence of herpes infection and disease appears to be associated with high frequency of HLA-A(∗)24, HLA-B(∗)27, HLA-B(∗)53 and HLA-B(∗)58 alleles.
136	24798939	Associations of HLA-A, HLA-B and HLA-C alleles frequency with prevalence of herpes simplex virus infections and diseases across global populations: implication for the development of an universal CD8+ T-cell epitope-based vaccine.
137	24798939	The present report: (i) analyzes the prevalence of HSV-1 and HSV-2 infections across various regions of the world; (ii) analyzes potential associations of common HLA-A, HLA-B and HLA-C alleles with the prevalence of HSV-1 and HSV-2 infections in the Caucasoid, Oriental, Hispanic and Black major populations; and (iii) discusses how our recently developed HLA-A, HLA-B, and HLA-C transgenic/H-2 class I null mice will help validate HLA/herpes prevalence associations.
138	24798939	Overall, high prevalence of herpes infection and disease appears to be associated with high frequency of HLA-A(∗)24, HLA-B(∗)27, HLA-B(∗)53 and HLA-B(∗)58 alleles.
139	24995346	Distribution of HLA-A, -B, and -C alleles and HLA/KIR combinations in Han population in China.
140	24995346	A total of 27 HLA-A, 54 HLA-B, and 31 HLA-C alleles were found in this population.
141	24995346	The results of KIR/HLA-C combination analysis showed that all individuals had at least one inhibitory or activating KIR/HLA-C pair, and one KIR/HLA-C pair was the most frequent (157/239), followed by two pairs (46/239), three pairs (33/239), and no pairs (3/239).
142	24995346	Distribution of HLA-A, -B, and -C alleles and HLA/KIR combinations in Han population in China.
143	24995346	A total of 27 HLA-A, 54 HLA-B, and 31 HLA-C alleles were found in this population.
144	24995346	The results of KIR/HLA-C combination analysis showed that all individuals had at least one inhibitory or activating KIR/HLA-C pair, and one KIR/HLA-C pair was the most frequent (157/239), followed by two pairs (46/239), three pairs (33/239), and no pairs (3/239).
145	26453750	Human cells expressing HLA class I ligands for inhibitory receptors KIR2DL1, KIR2DL2/3, or CD94-NKG2A were transfected with IL-15Rα.
146	26453750	Proliferation of primary NK cells in response to transpresented IL-15 was reduced by engagement of either KIR2DL1 or KIR2DL2/3 by cognate HLA-C ligands.
147	26453750	Inhibitory KIR-HLA-C interactions did not reduce the proliferation induced by soluble IL-15.
148	26453750	Therefore, transpresentation of IL-15 is subject to downregulation by MHC class I-specific inhibitory receptors.
149	26453750	Similarly, proliferation of the NKG2A(+) cell line NKL induced by IL-15 transpresentation was inhibited by HLA-E.
150	26453750	Coengagement of inhibitory receptors, either KIR2DL1 or CD94-NKG2A, did not inhibit phosphorylation of Stat5 but inhibited selectively phosphorylation of Akt and S6 ribosomal protein.
151	26453750	Human cells expressing HLA class I ligands for inhibitory receptors KIR2DL1, KIR2DL2/3, or CD94-NKG2A were transfected with IL-15Rα.
152	26453750	Proliferation of primary NK cells in response to transpresented IL-15 was reduced by engagement of either KIR2DL1 or KIR2DL2/3 by cognate HLA-C ligands.
153	26453750	Inhibitory KIR-HLA-C interactions did not reduce the proliferation induced by soluble IL-15.
154	26453750	Therefore, transpresentation of IL-15 is subject to downregulation by MHC class I-specific inhibitory receptors.
155	26453750	Similarly, proliferation of the NKG2A(+) cell line NKL induced by IL-15 transpresentation was inhibited by HLA-E.
156	26453750	Coengagement of inhibitory receptors, either KIR2DL1 or CD94-NKG2A, did not inhibit phosphorylation of Stat5 but inhibited selectively phosphorylation of Akt and S6 ribosomal protein.