Relevant bibliographies by topics / HLA-DP

Academic literature on the topic 'HLA-DP'

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Published: 10 December 2022
Last updated: 9 March 2023

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Journal articles on the topic "HLA-DP"

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Amar, A., G. T. Nepom, E. Mickelson, H. Erlich, and J. A. Hansen. "HLA-DP and HLA-DO genes in presumptive HLA-identical siblings: structural and functional identification of allelic variation." Journal of Immunology 138, no. 6 (March 15, 1987): 1947–53. http://dx.doi.org/10.4049/jimmunol.138.6.1947.

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Abstract We analyzed HLA class II genomic polymorphisms in three families in which bone marrow transplantation was performed between individuals presumed to be HLA identical, but in which unexplained mixed lymphocyte culture reactivity was observed. These families were characterized by classical HLA serology, MLC, and DP typing. In each family, a pair of "HLA-identical" siblings demonstrated a small proliferative response in bidirectional MLC. Southern blotting analysis performed with cDNA probes for DQ alpha, DP alpha, and DP beta identified DP genomic differences in each case. Hybridization of Bgl II-digested genomic DNA with a DP alpha cDNA probe revealed three prominent polymorphic fragments (7.7, 5.8, and 3.7 kb), which discriminated between presumptive identical siblings and indicated crossover events within HLA. Similarly, hybridization of SstI-digested genomic DNA with a DP beta cDNA probe, although resulting in a more complex pattern, identified DP genomic disparity between the presumed HLA identical siblings. Hybridization of SstI-digested DNA from two families with evidence of DP recombination was performed by using an oligonucleotide probe specific for the newly described HLA class II gene DO beta. Two major polymorphic fragments, at 6.2 and 3.3 kb, segregated in these families and localized the crossovers flanking the DO beta gene between the DQ and DP loci. The contribution of the antigenic differences marked by these HLA DP and DO DNA polymorphisms to allorecognition in MLR and in graft-vs-host disease are discussed.
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Pawelec, G., P. Reekers, D. Brackertz, D. Sansom, E. M. Schneider, M. Blaurock, C. Müller, A. Rehbein, I. Balko, and P. Wernet. "HLA-DP in rheumatoid arthritis." Tissue Antigens 31, no. 2 (February 1988): 83–89. http://dx.doi.org/10.1111/j.1399-0039.1988.tb02068.x.

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Marie-Marthe, Tongio, van den Berg Loonen Ella, Bignon Chandanayingyong, Chandanayingyong Dasnayanee, Dormoy Anne, Eiermann Thomas, Marshall William, Park Min Sik, and GMTh Schreuder. "HLA-DP detected by serology." Human Immunology 47, no. 1-2 (April 1996): 97. http://dx.doi.org/10.1016/0198-8859(96)85222-0.

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Mitsuishi, Y., K. Bibee, J. Hopfield, and P. I. Terasaki. "HLA-DP polymorphism in blacks." Human Immunology 40 (January 1994): 70. http://dx.doi.org/10.1016/0198-8859(94)91798-1.

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Laghmouchi, Aicha, Conny Hoogstraten, Peter Van Balen, Rick van de Water, Marian van de Meent, J. H. Frederik Falkenburg, and Inge Jedema. "The Allo-HLA-DP Restricted T Cell Repertoire Contains a Variety of Tissue-Restricted Specificities with Therapeutic Value." Blood 128, no. 22 (December 2, 2016): 3356. http://dx.doi.org/10.1182/blood.v128.22.3356.3356.

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Abstract T cell-depleted allogeneic stem cell transplantation (alloSCT) is applied in patients with hematological malignancies to reduce the risk of graft versus host disease (GvHD), but the associated increased risk of infections and disease relapse makes scheduled donor-lymphocyte-infusion (DLI) necessary. Since HLA-DP is not taken into account in the matching procedure, stem cell grafts from unrelated donors are often only 10/10 matched, and mismatched for HLA-DP. Under non-inflammatory conditions, expression of HLA-DP is restricted to hematopoietic cells. Therefore, treatment with HLA-DP mismatched donor CD4 T cells can induce a specific graft versus leukemia (GvL) effect. However, in some cases, patients receiving HLA-DP mismatched CD4 T cells suffer from GvHD mediated by a profound allo-HLA-DP specific immune response. Adoptive transfer of in-vitro selected allo-HLA-DP restricted donor T cells directed against antigens specifically expressed on hematopoietic cells may be an elegant strategy to induce a specific GvL effect without coinciding GvHD. To investigate the feasibility of this approach, the allo-HLA-DP restricted T cell repertoire was dissected to unravel potential tissue specificities and to investigate the presence of hematopoiesis-specific CD4+ T cells with therapeutic value within this compartment. To induce allo-HLA-DP directed T cell responses, HLA-DP mismatched (10/10 matched) donor/patient pairs were selected. Donor PBMC were co-cultured with patient mature monocyte-derived dendritic cells (DC) for 14 days. The donor cells were first re-stimulated with autologous DC and depleted of activated auto-reactive CD137+ T cells using magnet cell separation (MACS). The negative fraction was then stimulated with the HLA-DP mismatched patient DC to induce activation of allo-reactive T cells. These allo-reactive CD137+ CD4+ T cells were clonally isolated using flowcytometric cell sorting, and expanded. Allo-HLA-DP restricted recognition of different hematopoietic and non-hematopoietic stimulator cells by the T cell clones was assessed using IFNγ and IL-4 ELISA. The T cells were tested against a large panel of hematopoietic cells (monocytes, DC, EBV-LCL and PHA blasts) of donor and patient origin, leukemic cell samples (AML) and non-hematopoietic cells (IFNγ pretreated, HLA-class-II expressing, skin-derived fibroblasts, and target-HLA-DPB1-transduced HELA, lung, kidney, and colon carcinoma cell lines). After re-stimulation with patient DC, flowcytometry showed frequencies of 0.5-10% of allo-DC activated (CD137+) CD4+ T cells. After cell sorting 1521 T cell clones from 4 different HLA-DP mismatched patient/donor pairs were tested against donor EBV-LCL, donor DC, patient EBV-LCL and patient DC as initial screening for allo-reactivity. 80% of the T cell clones showed allo-reactivity, as defined by recognition of patient, but not donor-derived EBV-LCL and/or DC. 14% of the tested clones showed no reactivity and 6% were auto-reactive. The HLA-DP restriction was analyzed of 400 selected allo-reactive T cell clones, using a panel consisting of donor, patient and 3rd party EBV-LCL or DC, 3rd party fibroblasts and target HLA-DPB1 transduced HELA cells. Of these 400 T cell clones, 65% were confirmed to be HLA-DP restricted. From these allo-HLA-DP restricted T cell clones 80% recognized both hematopoietic and non-hematopoietic cells expressing the target allo-HLA-DPB1. The other 20% of the allo-HLA-DP restricted T cell clones only produced cytokines when stimulated with hematopoietic cells (EBV-LCL and/or DC), and not when stimulated with non-hematopoietic cells (Fibroblasts, HELA, carcinoma cell lines). Moreover, 40% of these T cell clones showing hematopoiesis-restricted recognition only recognized DC, but not EBV-LCL expressing the target HLA-DPB1 allele. These clones also recognized primary AML blasts and proliferating CD34+ progenitor cells, illustrating a myeloid lineage restricted recognition pattern. These results illustrate that reactivity of allo-HLA-DP restricted T cells is not only determined by the expression of the target HLA-DPB1 allele, but is also dictated by cell lineage-specific gene expression causing differential peptide expression in HLA-DPB1. As a result, a significant portion of the allo-HLA-DP specific T cell repertoire harbors a specific GvL recognition pattern with high therapeutic value. Disclosures No relevant conflicts of interest to declare.
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Miyadera, Hiroko, Yuki Okabe, Cindy Chen, Katsushi Tokunaga, and Masashi Mizokami. "A large scale screening of HLA-class II-binding peptides from HBs and HBc peptide libraries." Journal of Immunology 196, no. 1_Supplement (May 1, 2016): 185.2. http://dx.doi.org/10.4049/jimmunol.196.supp.185.2.

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Abstract Objectives Variations in the human leukocyte antigens (HLA)-DP are associated strongly with susceptibility/protection to chronic hepatitis B virus (HBV) infection. It has been reported previously that HLA-DPB1*05:01 and *09:01, the major HLA-DP alleles in East Asians, are associated with susceptibility, while HLA-DPB1*04:01 and *04:02, the major alleles in Europeans, confer protection against chronic hepatitis B (Kamatani, et al. Nat Genet (2009); Nishida, et al. PLoS One (2012)). To identify the peptides that are potentially involved in immunological responses against HBV infection, we screened the peptide libraries of the HBV surface antigen (HBs) and core antigen (HBc) through the cell-surface HLA expression assay. Methods The six major HLA-DP haplotypes that are associated with susceptibility to or protection against chronic hepatitis B were used in this study. Peptide libraries were designed for the entire HBs and HBc antigens, based on the consensus sequence of the genotype C. To identify the HLA-DP-binding region, we expressed HLA-DP in fusion with each peptide, using fibroblast cell line as an expression host. Result The level of HLA-peptide interaction was estimated by measuring the level of cell-surface expression of each HLA-peptide fusion construct. Out of >70 peptides that cover the entire HBs and HBc antigens, we found several regions that bound strongly to certain HLA-DP allele products. In this presentation we show an overview of the methodology and discuss potential mechanisms that might underlie association of HLA-DP with chronic hepatitis B.
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Kawase, Takakazu, Keitaro Matsuo, Koichi Kashiwase, Hidetoshi Inoko, Hiroh Saji, Shunichi Kato, Takehiko Sasazuki, Yoshihisa Kodera, and Yasuo Morishima. "Identification of HLA Allele Mismatch Combinations and Amino Acid Substitution Positions Associated with GVL Effect after Unrelated HSCT: Analysis from the Japan Marrow Donor Program." Blood 110, no. 11 (November 16, 2007): 44. http://dx.doi.org/10.1182/blood.v110.11.44.44.

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Abstract Graft-versus-leukemia (GVL) effect is considered to reduce relapse rate due to eradication of residual leukemia cells after allogeneic hematopoietic stem cell transplantation (HSCT). Segregation it from graft-versus-host disease (GVHD) has been main issue clinically. We recently clarified 16 high-risk HLA mismatch combinations and eight high-risk specific amino acid substitution positions for severe acute GVHD in six HLA loci. In the current study, we clarified HLA allele mismatch combinations and amino acid substitution positions associated with GVL effect. Consecutive 4643 patients transplanted for hematological malignancy (ALL, AML, CML, MDS, MM and ML) with T cell replete marrow from a serologically HLA-A, -B and -DR antigen-matched donor through Japan Marrow Donor Program were registered in this cohort study. All HLA-A, -B, -C, -DRB1, -DQB1 and -DPB1 alleles were retrospectively typed. The effect of HLA locus mismatch in allele level, the HLA allele mismatch combinations in HLA six loci and amino acid substitution positions on reduced relapse rate was analyzed using a multivariable competing risk regression model. As results (1) Mismatches of HLA-C (Odds ratio (OR)=0.69; p<0.0001) and HLA-DPB1 (OR=0.78; p<0.0001) were strongly reduced leukemia relapse, and HLA-A (OR=0.99; p=0.9), HLA-B (OR=0.98; p=0.91), HLA-DRB1 (OR=0.93; p=0.54) and HLA-DQB1 (OR=1.06; p=0.54) were not. (2) Total 10 HLA mismatch combinations were significantly associated with GVL effect; four in HLA-C allele (donor Cw*0303- patient Cw*1502 (n=25) OR=0.23, Cw*0102-Cw*1402 (n=16) OR=0, Cw*0801-Cw*0102 (n=10) OR=0 and Cw*1402-Cw*0304 (n=23) OR=0), six in HLA-DPB1 allele (DP*0402-DP*0201 (n=66) OR=0.41,?DP*0501-DP*0201 (n=351) OR=0.7,?DP*0501-DP*0401 (n=53) OR=0.45,?DP*0501-DP*0402?(n=121) OR=0.59, DP*0901-DP*0201 (n=50) OR=0.38 and DP*1301-DP*0201 (n=21) OR=0), but none in HLA-A, -B, -DRB1 and -DQB1 allele. Except two of four combinations in HLA-C, the other two in HLA-C and all six in HLA-DPB1 were different from high-risk one for severe acute GVHD. (3) Specific amino acid substitution at positions 9, 99, 156 in HLA-C molecule was elucidated as significant factors responsible for GVL effect and one of three was different from substitutions responsible for severe acute GVHD. As for HLA-DPB1, no significant association between the positions of specific amino acid substitution and GVL were found. In conclusion, large scale comprehensive analysis made it possible to identify 4 HLA-C and 6 HLA-DPB1 mismatch combinations responsible for GVL effects, some of which are different from one responsible for acute GVHD. Responsible amino acid substitutions on specific position were also elucidated in HLA-C, but not in HLA-DPB1. These findings suggest that donor selection according to these results could segregate GVL from acute GVHD, therefore these strategies might be beneficial for the selection of suitable donor for HSCT. And that, we speculate that the molecular base of GVL caused by the HLA-DPB1 mismatch might be different from that in HLA-C.
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Cheng, Lin, Yan Guo, Shipeng Zhan, and Peiyuan Xia. "Association between HLA-DP Gene Polymorphisms and Cervical Cancer Risk: A Meta-Analysis." BioMed Research International 2018 (June 13, 2018): 1–13. http://dx.doi.org/10.1155/2018/7301595.

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Objective. We aimed to derive a more precise estimation of the associations between human leukocyte antigens DP (HLA-DP) gene polymorphisms and cervical cancer risk by meta-analysis. Methods. PubMed, EMBASE, ScienceDirect, Web of Science, Chinese National Knowledge Infrastructure (CNKI), and Wanfang databases were systematically searched to identify studies investigating the relationship between HLA-DP gene polymorphisms and cervical cancer. The associations between them were evaluated by pooled OR and 95% CI. Results. A total of 11 studies including 5008 cases and 9322 controls with 11 HLA-DP alleles were included in the current meta-analysis. Results. The results showed that HLA-DPB1⁎03:01 was significantly associated with an increased risk of cervical cancer (OR=1.252, 95%CI: 1.116-1.403, Pz=0.001), while HLA-DPB1⁎04:02 and HLA-DP rs3117027 G allele were significantly associated with a decreased risk of cervical cancer (OR=0.744, 95%CI: 0.652-0.848, Pz=0.001; OR=0.790, 95%CI: 0.745-0.837, Pz=0.001), and HLA-DP rs9277535 G allele was significantly associated with a decreased risk of cervical cancer in Asia (OR=0.802, 95%CI: 0.753-0.855, Pz=0.001). Subgroup analyses based on race system showed that HLA-DPB1⁎13:01 was significantly associated with an increased risk of cervical cancer in Asia (OR=1.834, 95%CI: 1.107-3.039, Pz=0.019). No significant association was established for the HLA-DP following alleles: DPB1⁎02:01, DPB1⁎02:02, DPB1⁎04:01, DPB1⁎05:01, rs4282438, and rs3077. Conclusion. HLA-DP gene polymorphisms (HLA-DPB1⁎03:01, DPB1⁎04:02, DPB1⁎13:01, rs9277535, and rs3117027) were significantly associated with cervical cancer.
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Rutten, Caroline E., Simone A. P. van Luxemburg-Heijs, Inge Jedema, Mirjam Heemskerk, Roelof Willemze, and J. H. Frederik Falkenburg. "Complete Remission of Immunocytoma without Graft Versus Host Disease Caused by Allo-HLA-DP Specific T Cells." Blood 108, no. 11 (November 16, 2006): 3665. http://dx.doi.org/10.1182/blood.v108.11.3665.3665.

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Abstract Mismatching for HLA-DPB1 in unrelated donor hematopoietic stem cell transplantation (URD-SCT) has been associated with a significant decreased risk of disease relapse, indicating that HLA-DP might be a target for a graft versus leukemia (GVL) effect in HLA-class II expressing hematological malignancies. To determine whether a specific GVL effect could be caused by allo-HLA-DP specific T cells, we analyzed the immune response in a patient with a refractory immunocytoma responding to donor lymphocyte infusion (DLI) after HLA-DP mismatched URD-SCT. Patient and donor were fully matched for HLA-A, -B, -C, -DR and -DQ, but differed for both HLA-DP alleles (donor HLA-DPB1*0402/0501; patient HLA-DPB*020102/0301). The patient received a T cell depleted URD-SCT after a non-myeloablative conditioning regimen, resulting in mixed chimerism (75% donor) without GVHD. Because of a hematological relapse, a single DLI was given 6 months after SCT, resulting in a profound anti-leukemic effect with only grade I GVHD, treated with topical corticosteroids. 6 weeks after DLI, malignant cells in peripheral blood (PB) had dropped from 72% to 47%. 7 weeks later, only 3% malignant cells were present, and after 4 months, complete remission and conversion to full donor chimerism in the absence of GVHD was observed. To determine whether allo-HLA-DP specific T cells were involved in the immune response, leukemia-reactive donor T cell clones were isolated from PB or bone marrow at different time points during the response to DLI. Patient derived T cells were overnight stimulated with irradiated leukemic cells harvested before transplantation, and clonal IFNγ producing T cells were sorted and expanded. 21 CD4+ T cell clones, 19 CD8+ T cell clones and 6 NK cell clones were tested for recognition of patient or donor derived cells as measured by IFNγ production and cytotoxic activity. The CD8+ or NK clones did not recognize patient leukemic cells. However, all 21 CD4+ clones produced INFγ in response to patient leukemic cells but not to donor cells. To determine whether these CD4+ T cell clones were capable of killing the leukemic cells, a CFSE based cytotoxicity assay was performed. 8 clones showed 30–90% lysis of the leukemic cell population. To further analyze the specificity of these CD4+ clones, blocking and panel studies were performed. Blocking with the HLA-DP specific mAb B7.21 abrogated IFNγ production by all clones, confirming HLA-DP restricted recognition. A panel study using 12 unrelated EBV-LCL expressing different HLA-DP alleles identified 18 clones specific for HLA-DPB1*0301, and 3 clones specific for HLA-DPB1*0201. To analyze the polyclonality of the immune response, the distribution of TCR Vβ chains was characterized by RT-PCR and sequence reactions. 7 different Vβs were found within the HLA-DPB1*0301 specific clones and 3 different Vβs within the HLA-DPB1*0201 specific clones. T cells using the same Vβ could be isolated at different time points during the clinical response, demonstrating the significance of this anti-HLA-DP response. In conclusion, we observed in a patient with an HLA-class II positive B cell malignancy a profound GVL effect without GVHD, caused by a polyclonal immune response comprising both T helper and cytotoxic CD4+ HLA-DP specific T cell clones directed against both HLA-DP alleles. These data indicate that in HLA-class II expressing hematological malignancies HLA-DP mismatched SCT may be preferable over a fully matched SCT making use of HLA-DP as a specific target for immunotherapy.
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Tu, C. F., T. Sato, M. Hagihara, K. H. Lee, Y. C. Lee, C. N. Weng, R. M. Chu, K. Tsuji, and C. J. Lee. "Expression of HLA-DP antigen on peripheral blood mononuclear cells of HLA-DP transgenic pigs." Transplantation Proceedings 30, no. 7 (November 1998): 3502–3. http://dx.doi.org/10.1016/s0041-1345(98)01114-2.

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Dissertations / Theses on the topic "HLA-DP"

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Barker, Anna. "The role of HLA-DP in renal transplantation." Thesis, University of Manchester, 2008. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.492281.

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Introduction: HLA-DP (DP) is a human Major Histocompatibility Complex class II molecule which presents peptide to the immune system. In the context of kidney transplantation, DP mismatches (mm) can be recognised as allogeneic, demonstrated by the detection of DP specific antibodies (abs). IFN-y is produced during the inflammatory response following kidney transplantation and induces cell surface expression of HLA-c1ass II molecules, providing non-self target molecules for the binding of abs and subsequent graft damage. This study aimed to address the hypotheses that DP mm affect kidney transplant (tx) survival, DP abs are produced. against mismatched donor antigens and are clinically relevant, DP expression can be upregulated in cell types involved in tx rejection and binding of abs to class II molecules leads to the activation of cell signalling pathways which contribute to the mechanism of chronic rejection (CR). Methods: 147 recipients of txs with zero mms at HLA-A, B and DR (000 txs) were DPB1 typed and 127 were DPA1 typed. The effect of mismatching at both loci was investigated using Kaplan-Meier survival analysis and multivariate Cox proportional hazards analysis. 123 of the recipients were tested for class II and DP abs using FlowPRA® assays (One Lambda) and their clinical significance analysed. HLA-DPA1 and B1 gene expression was investigated in IFN-y treated Human Microvascular Endothelial Cells (HMEC) and HK-2 cells (a renal epithelial cell line) using quantitative real-time reverse transcriptase PCR (q r-t RT-PCR). The effect of IFN-y treatment on HMEC DP cell surface expression was determined using flow cytometry. IFN-y-treated HMEC were investigated for cell activation in response to HLA ab binding using a plate fluorimetry method to detect changes in intracellular calcium levels ([Ca2+]i). HMEC protein expression in response to DP ab binding was investigated using an antibody array (Sigma). Results: DPA1 mm had no effect on graft survival whereas an effect of DPB1 mm was demonstrated in retransplant patients using Cox regression analysis (p = 0.04). DP abs were detected in 11 of 40 (27.5%) patients with class II abs. DP abs were frequently found in patients who had had more than one transplant (7/11) and in pre-ODD tx samples (10/11). Six of the 11 recipients had no DP mms at their 000 tx. DP abs were produced in response to previous transplant or pregnancy. The DP response was restimulated by repeat DP mm and in one case was implicated in tx rejection and in another with tx rejection and graft loss. DP gene and cell surface expression increased in response to IFN-y treatment. Cell activation measured by [Ca2+]i increase was observed after class I and class II ab binding. DP ab binding to HMEC led to increased expression of a variety of proteins inclUding those involved in apoptosis, cell cycle and signal transduction. Summary and Conclusion: This study has shown that DP does have a role in renal transplantation. DPB1 mms affect survival of re-transplants. DP abs are produced and reactivated in response to repeat DP mm and were implicated in graft loss. DP gene and cell surface expression was induced on epithelial and endothelial cell lines and DP ab binding led to cell activation. DP ligation on HMEC also led to increased expression of proteins previously shown to be involved in class I ab-mediated cell signalling pathways in endothelial cells. The results of this study suggest that all kidney tx candidates who have had a preVious transplant or pregnancy should be tested for DP abs in order to inform donor selection and patient management.
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Sage, Deborah Anne. "HLA-DP immunogenetics and significance in allogeneic bone marrow transplantation." Thesis, University of Portsmouth, 1996. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.308955.

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Baudeau, Christophe. "Antigenes de classe ii hla-dp : structure, fonction, polymorphisme : revue de la litterature et contribution personnelle a l'etude de l'expression sur les tissus normaux et pathologiques." Université Louis Pasteur (Strasbourg) (1971-2008), 1991. http://www.theses.fr/1991STR1M152.

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Essaket, Soumia. "Alloréaction chez l'homme : spécificité de clones de lymphocytes T et structure primaire des molécules HLA-DR et HLA-DP." Toulouse 3, 1990. http://www.theses.fr/1990TOU30240.

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Les alloantigenes hla de classe ii sont des glycoproteines de surface codees par des loci situes dans la region hla-d: hla-dr; dq et dp. Ces molecules du complexe majeur d'histocompatibilite agissent comme elements de restriction en presentant les fragments peptidiques aux lymphocytes t. Le modele tridimensionnel hypothetique des molecules hla de classe ii suggere que le premier domaine de chacune des chaines alpha et beta forment ensemble une crevasse constituee de feuillets et de deux helices formant respectivement le plancher et les bords. Les resultats obtenus avec des clones de lymphocytes, diriges contre les specificites drw13, dpw3 et certaines specificites dp non encore definies, nous ont permis de localiser les sites fonctionnels sur ces molecules. La correlation entre les reponses proliferatives des clones de lymphocytes t anti-dr et anti-dp et les sequences primaires du premier domaine de ces molecules montre que les residus situes aussi bien au niveau des helices qu'au niveau des feuillets peuvent influencer la reconnaissance par les lymphocytes y. Des donnees recentes, obtenues par plusieurs groupes, montrent que dans le cas de l'alloreaction de lymphocyte t alloreactif reconnait un complexe forme par la molecule hla etrangere et un peptide du soi. Nos resultats obtenus avec un clone t, teste dans differentes conditions experimentales, suggerent que la stimulation des lymphocytes t alloreactifs necessite aussi bien la molecule hla etrangere qu'un peptide du soi qui peut provenir de al degradation des molecules hla elles-memes. Nous avons observe que ce peptide hla peut provenir d'une autre cellule (experience de melange de cellules a1 et dpw3 positives) et meme etre apporte par un surnageant filtre. Le fait que les cellules presentant l'antigene peuvent internaliser et degrader les molecules hla des cellules voisines peut avoir des implications en transplantation clinique
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Zwerger, Michael [Verfasser], and Simone [Akademischer Betreuer] Thomas. "Charakterisierung eines HLA-DP spezifischen T-Zell Rezeptors / Michael Zwerger ; Betreuer: Simone Thomas." Regensburg : Universitätsbibliothek Regensburg, 2018. http://d-nb.info/1172071780/34.

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Vatter, Sarah [Verfasser], and Wolfgang [Akademischer Betreuer] Herr. "HLA-DP-spezifische T-Zell-Rezeptoren als Immuntherapeutika zur Behandlung der akuten myeloischen Leukämie / Sarah Vatter ; Betreuer: Wolfgang Herr." Regensburg : Universitätsbibliothek Regensburg, 2018. http://d-nb.info/1163109118/34.

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DORMOY, ANNE. "Etude du polymorphisme des genes a1 et b1 de la molecule d'histocompatibilite hla-dp par differentes techniques de biologie moleculaire." Université Louis Pasteur (Strasbourg) (1971-2008), 1991. http://www.theses.fr/1991STR13120.

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L'identite des molecules de classe deux du complexe majeur d'histocompatibilite (cmh) de l'homme (dr? dq et dp) conditionne le devenir des allogreffes. Pour selectionner au mieux les paires donneurs-receveurs de moelle osseuse non apparentes (dr et dp identiques), le polymorphisme des genes dp doit etre defini. Dans ce travail, differentes techniques de biologie moleculaire applicables a la determination des alleles dp ont ete utilisees: 1) analyse du polymorphisme des fragments de restriction (rflp) de la region dp contenant deux genes et deux pseudogenes; 2) typage par hybridation au nucleotide pres, d'olisosondes specifiques du deuxieme exon polymorphique du gene dpb1 amplifie par pcr; 3) analyse du rflp obtenu par digestion de ce meme exon amplifie (pcr-rflp); 4) sequencage et les resultats obtenus analyses comparativement a ceux de la technique de reference de typage cellulairte plt (primed lymphocyte test) (126 individus etudies). Les conclusions suivantes ont ete obtenues: 1) l'oligotypage (ou le pcr-rflp) sont conseilles pour le groupage dp en routine: leurs resultats (confirmes par le sequencage dans certains cas) corroborent presque a 100% ceux obtenus par plt; 2) l'analyse par rflp ne peut etre utilisee dans ce but; basee sur l'existence d'une liaison entre des sites de restriction localises dans la region dp (70kb) et les alleles de l'exon polymorphique du gene dpb1, 20% des resultats apportes par cette technique different de ceux obtenus par plt ou oligotypage. Ces donnees conduisent a la definition de nouveaux haplotypes dp probablement generes par des phenomenes de conversion genique entre chromosomes homologues
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BOUVET, MARIE-ANDREE. "Etude par technique pcr (polymerase chain reaction) du polymorphisme hla dr, dq, dp dans la polyarthrite rhumatoide et dans son expression clinique." Rennes 1, 1992. http://www.theses.fr/1992REN1M147.

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CRIVELLO, PIETRO. "New molecular insights into HLA immunogenicity." Doctoral thesis, Università degli Studi di Milano-Bicocca, 2012. http://hdl.handle.net/10281/29854.

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Alloreactivity is the major barrier to solid organ and hematopoietic stem cell transplantation (HSCT), determining important clinical events such as graft rejection and graft versus host disease. This biological phenomenon is due to the immunogenicity of allogeneic Human Leukocyte Antigens (HLA) expressed in transplanted tissues and recognized by T cell receptor (TCR) on the surface of alloreactive T cells. In the past, the hosting laboratory identified an immunogenic T cell epitope (TCE) encoded by a subset of HLA-DPB1 alleles, thereby defining permissive and non-permissive DPB1 mismatches between donor and recipient associated with different clinical outcomes after HSCT. Aim of this thesis is to elucidate the molecular basis underlying the different clinical impact of DPB1 mismatches in order to improve our understanding of HLA immunogenicity in the context of transplantation. To achieve this aim, we investigated if the clinical effect of DPB1 mismatches was reflected by the strength of their in vitro alloreactive T cell response and, subsequently, we characterized the alloreactive response to one of the most immunogenic DPB1 alleles, HLA-DPB1*09:01 (HLA-DP9), at the molecular level by homology modeling driven site directed mutagenesis. The strength of the alloreactive T cell response to HLA-DP was assessed in Mixed Lymphocyte Reactions between healthy responder/stimulator pairs mismatched only at the DPB1 locus, followed by quantitative assessment of responder T cells upregulating the cell surface activation marker CD137. We observed significantly higher frequencies of activated T cells against non-permissive mismatches (n=9; mean 10.13% ± 7.51%) compared to permissive mismatches (n=15; mean 2.34% ± 2.82% p<0.05). SDM of HLA-DP9 was performed on 6 polymorphic amino acid residues predicted to be crucial for interaction with bound peptide (positions 9, 35, 55, 69, 76 and 84), and on 2 amino acid residues putatively involved in direct interaction with the TCR (positions 56 and 57). These residues were mutated into amino acids naturally occurring in other HLA-DP variants. A lentiviral vector expression platform was used to express the wild type or mutant HLA-DP in 2 HLA homozygous reporter B lymphoblastoid Cell lines. A panel of 8 alloreactive T cell effectors, specific for wild type HLA-DPB1*09:01 (n=6) or for DPB1*10:01 and DPB1*1701, respectively, but crossreactive to DPB1*09:01 (n=2), was used to evaluate the impact of mutagenesis on T cell recognition by gIFN ELISpot or CD107a degranulation assay. For T cells specifically alloreactive to HLA-DPB1*09:01, recognition was influenced by a complex pattern of residues, which was different for each of the 6 effectors studied. In contrast, for the 2 T cells cross-reactive to HLA-DPB1*09:01, only 2 amino acids (positions 69 and 76) had an influence on allorecognition, suggesting the presence of a more restricted set of T cell epitopes in the context of cross-reactivity rather than nominal specificity. These results are consistent with the peptide involvement in alloreactivity to HLA-DPB1*09:01, and underline the complexity of allorecognition which may be one of the mechanisms underlying the immunogenicity of this molecule. Finally, an additional collaborative study with the North Italian Program for Solid Organ Transplantation was aimed at predicting the functional role of amino acid point mutations in newly described naturally occurring variants of HLA-A3 and A32, respectively, by homology modeling. These studies confirmed data from the literature suggesting a relevant putative role of amino acid substitutions at positions 114 and 116, present in a variant of HLA-A3, on the molecular shape and charge of the peptide binding groove. In contrast, point mutations at position 151 and 258 found in two variants of HLA-A32 and A3, respectively, were not predicted to have important functional impacts, due to limited structural or biochemical changes of the groove. In conclusion, our results shed new light on the molecular basis of T cell alloreactivity. In particular, we showed that the stronger immunogenicity of non-permissive DPB1 mismatches is reflected by a divergent and complex T cell epitope repertoire with a putative involvement of the peptide repertoire presented to the alloreactive TCRs. Identification of specific allopeptides associated with these responses will allow to further dissect their molecular basis.
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Triebel, Frédéric. "Analyse fonctionnelle et structurale des antigènes membranaires ayant un rôle dans la réponse proliférative de clones lymphocytaires T humains spécifiques de l'anatoxine diphtérique." Paris 6, 1986. http://www.theses.fr/1986PA066147.

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Books on the topic "HLA-DP"

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Sage, Deborah Anne. HLA-DP immunogenetics and significance in allogeneic bone marrow transplantation. Portsmouth: University of Portsmouth, School of Biological Sciences, 1996.

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Book chapters on the topic "HLA-DP"

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Sanchez-Perez, M., and S. Shaw. "HLA-DP: Current Status." In HLA Class II Antigens, 83–108. Berlin, Heidelberg: Springer Berlin Heidelberg, 1986. http://dx.doi.org/10.1007/978-3-642-70367-6_6.

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Hyldig-Nielsen, Jens Jorgen, and Arne Svejgaard. "Workshop Report for the HLA-DP Region." In Immunobiology of HLA, 867–76. New York, NY: Springer New York, 1989. http://dx.doi.org/10.1007/978-1-4612-3552-1_254.

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Bontrop, R. E., N. Otting, E. J. Baas, and M. J. Giphart. "Molecular Analysis of HLA-DP: DP β Chain Charge Heterogeneity Correlates with PLT Subtyping." In Immunobiology of HLA, 322. Berlin, Heidelberg: Springer Berlin Heidelberg, 1989. http://dx.doi.org/10.1007/978-3-662-39946-0_120.

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Ødum, Niels, Bodil K. Jakobsen, Niels Morling, Arne Svejgaard, Niels Jacobsen, and Lars Lamm. "HLA-DP and Acute Graft Versus Host Disease." In Immunobiology of HLA, 517–19. Berlin, Heidelberg: Springer Berlin Heidelberg, 1989. http://dx.doi.org/10.1007/978-3-662-39946-0_222.

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Marshall, W. H., S. Drover, D. Codner, J. Gamberg, M. D. Copp, H.-W. Liu, L. T. Deng, and H. B. Younghusband. "HLA-DP Epitope Typing Using Monoclonal Antibodies." In Immunogenetics: Advances and Education, 223–32. Dordrecht: Springer Netherlands, 1997. http://dx.doi.org/10.1007/978-94-011-5486-4_27.

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Niven, M. J., C. Caffrey, J. A. Sachs, P. G. Cassell, R. Gallagher, P. Kumar, H. Festenstein, and G. A. Hitman. "HLA-DP Region Is Relevant to Celiac Disease Susceptibility." In Immunobiology of HLA, 449–50. Berlin, Heidelberg: Springer Berlin Heidelberg, 1989. http://dx.doi.org/10.1007/978-3-662-39946-0_186.

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Fernandez, Nelson, Mario O. Labeta, Marcej Kurpisz, and Hilliard Festenstein. "A Novel HLA-Class II Molecule Distinct from HLA-DP/DQ/DR." In Immunobiology of HLA, 329–32. Berlin, Heidelberg: Springer Berlin Heidelberg, 1989. http://dx.doi.org/10.1007/978-3-662-39946-0_124.

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Park, Min Sik, Toshinao Takenouchi, Paul I. Terasaki, Richard Tonai, and Aida Barbetti. "HLA-DP Region Complexity by CDC, RFLP, and Cellular Assays." In Immunobiology of HLA, 311–14. Berlin, Heidelberg: Springer Berlin Heidelberg, 1989. http://dx.doi.org/10.1007/978-3-662-39946-0_116.

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Mickelson, E., N. Reinsmoen, F. M. Robbins, R. Hartzman, N. Ødum, A. Svejgaard, C. Farrell, et al. "HLA-Dw and HLA-DP Typing of the Reference Panel of B-Lymphoblastoid Cell Lines." In Immunobiology of HLA, 38–42. New York, NY: Springer New York, 1989. http://dx.doi.org/10.1007/978-1-4612-3552-1_4.

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Mearin, M. Luisa. "HLA-DR-DP and -DQ Antigens in Coeliac Disease." In Coeliac Disease, 27–34. Dordrecht: Springer Netherlands, 1991. http://dx.doi.org/10.1007/978-94-015-7943-8_5.

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Conference papers on the topic "HLA-DP"

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Silveira, Lori J., Erin McCanlies, Tasha Fingerlin, Michael Van Dyke, Peggy M. Mroz, Matthew Strand, Andrew Fontenot, Christine Schuler, Ainsley Weston, and Lisa Maier. "Chronic Beryllium Disease, HLA DPB1 And The DP Peptide Binding Groove." In American Thoracic Society 2011 International Conference, May 13-18, 2011 • Denver Colorado. American Thoracic Society, 2011. http://dx.doi.org/10.1164/ajrccm-conference.2011.183.1_meetingabstracts.a4823.

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Hermawan, JR, H. Winter, L. Strakeljahn, M. Schmitzer, A. Dick, N. Kneidinger, R. Schramm, et al. "Influence of Antibodies against HLA DQA/DP to Chronic Lung Allograft Dysfunction." In 27. Jahrestagung der Deutschen Gesellschaft für Thoraxchirurgie. Georg Thieme Verlag KG, 2018. http://dx.doi.org/10.1055/s-0038-1668390.

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Brentville, Victoria, Rachael Metheringham, Ian Daniels, Katherine Cook, Peter Symonds, Tracy Pitt, Wei Xue, Mohamed Gijon, and Lindy Durrant. "Abstract A027: HLA-DP restricted responses to citrullinated proteins are pre-existing in the memory pool and can be rapidly reactivated to provide good tumor therapy." In Abstracts: Second CRI-CIMT-EATI-AACR International Cancer Immunotherapy Conference: Translating Science into Survival; September 25-28, 2016; New York, NY. American Association for Cancer Research, 2016. http://dx.doi.org/10.1158/2326-6066.imm2016-a027.

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Reports on the topic "HLA-DP"

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Cesare Saltini, Massimo Amicosante. Analysis of HLA-DP association with beryllium disease susceptibility in pooled exposed populations. Office of Scientific and Technical Information (OSTI), December 2009. http://dx.doi.org/10.2172/969219.

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