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Journal articles on the topic 'HLA-DP'

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Published: 10 December 2022

Last updated: 9 March 2023

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1

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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2

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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3

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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4

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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5

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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6

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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7

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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8

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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9

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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10

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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11

Hyldig-Nielsen, J. J., N. Morling, N. Odum, L. P. Ryder, P. Platz, B. Jakobsen, and A. Svejgaard. "Restriction fragment length polymorphism of the HLA-DP subregion and correlations to HLA-DP phenotypes." Proceedings of the National Academy of Sciences 84, no. 6 (March 1, 1987): 1644–48. http://dx.doi.org/10.1073/pnas.84.6.1644.

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12

Pesando, J. M., L. Graf, and P. Hoffman. "HLA-DP can be expressed with or without -DR molecules on a malignant B cell line." Journal of Immunology 137, no. 6 (September 15, 1986): 1932–36. http://dx.doi.org/10.4049/jimmunol.137.6.1932.

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Abstract HLA class II molecules (HLA-DR, -DQ, -DP) appear to differ in their ability to serve as corecognition elements in antigen presentation to T lymphocytes. Expression of these molecules on the autologous malignant B cell lines BALM-3, -4, and -5 was studied by binding of alloantisera and by indirect immunofluorescence and immune precipitation performed with well-characterized monoclonal antibodies. The following phenotypes were identified: BALM-5, HLA-DR+, -DP+; BALM-4, HLA-DR-, -DP+; BALM-3, HLA-DR-, -DP-. When treated with phorbol acetate (TPA), all three cell lines synthesize and express both HLA-DR and -DP molecules, indicating that the structural genes for these molecules remain intact. Thus HLA-DP can be expressed with or without HLA-DR molecules. Immune precipitation studies of metabolically labeled BALM-4 cells detect HLA-DR molecules in cells from TPA-treated but not control cultures, suggesting that TPA acts by inducing the transcription and/or translation of the genes for these class II molecules. HLA-DP molecules are detected in cells from both BALM-4 cultures. Recent studies suggest that BALM-5 but not BALM-3 or BALM-4 cells are HLA-DQ positive. TPA also appears to induce expression of HLA-DQ molecules on the latter two cell lines. The unique class II phenotypes of these autologous B cell lines in the resting state therefore appear to reflect differences in their ability to execute discrete steps leading to the surface expression of individual class II molecules. Variable expression of individual class II molecules by different cell populations may affect their ability to present cell-associated antigens to T lymphocytes.

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13

Szewczuk, Zbigniew, Andrzej Wilczyński, Piotr Stefanowicz, Wioletta Fedorowicz, Ignacy Z. Siemion, and Zbigniew Wieczorek. "Immunosuppressory mini-regions of HLA-DP and HLA-DR." Molecular Immunology 36, no. 8 (June 1999): 525–33. http://dx.doi.org/10.1016/s0161-5890(99)00066-8.

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14

Weiskopf, Daniela, Alba Grifoni, Michael Angelo, Eugene Moore, John Sidney, Elizabeth J. Phillips, Simon Alexander Mallal, Aruna D. de Silva, Bjoern Peters, and Alessandro Sette. "Characterization of HLA-DP and DQ restricted dengue virus-specific CD4+T cell responses reveals lower magnitude responses associated with a differential pattern of immunodominance as compared to DR restricted responses." Journal of Immunology 202, no. 1_Supplement (May 1, 2019): 140.14. http://dx.doi.org/10.4049/jimmunol.202.supp.140.14.

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Abstract Background Assessment of adaptive immunity is an important element to understand immunopathology and to define the correlates of protection against dengue virus (DENV). While previous studies characterized responses restricted by the HLA DRB1 locus, the responses associated with the DP and DQ loci have not been characterized to date. Accordingly, here we mapped HLA DP and DQ restricted DENV-specific CD4 T cell epitopes in PBMCs from individuals previously exposed to DENV from the general population of the Sri Lanka. Methods We studied the DP (*0101, *0201, *0401, *0402) and DQ (*0501, *0602, *0301, *0302, *0201) allelic variants which provide a greater than 80% population coverage worldwide. CD4+ T cells purified by magnetic bead negative selection were cultured for two weeks with autologous APC and pools of HLA –specific predicted binders and tested for reactivity in a standard IFNγ ELISPOT assay. Results Magnitude of responses for both the DP and DQ loci were significantly lower than previously observed for the DRB1 locus. This was correlated with lower membrane expression of HLA- DP and DQ molecules on the PBMCs as compared to HLA DR. While responses against Capsid were dominant for the various DR and DP alleles this protein was hardly recognized by DQ alleles. Responses against NS3 were dominant in the case of DR and DQ but absent in the case of DP, and response to NS1 were prominent in the case of the DP alleles, but negligible in the case of the DR and DQ alleles tested. Conclusion The HLA DP and DQ loci mediate DENV-CD4 specific immune responses of lower magnitude as compared to HLA DRB1. The responses mediated by the DP and DQ loci are also associated with distinct and characteristic patterns of immunodominance.

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Pesando, J. M., and L. Graf. "Differential expression of HLA-DR, -DQ, and -DP antigens on malignant B cells." Journal of Immunology 136, no. 11 (June 1, 1986): 4311–18. http://dx.doi.org/10.4049/jimmunol.136.11.4311.

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Abstract HLA class II antigens mediate interactions among cells involved in the immune response and play an important role in the process of self recognition. We made use of conventional alloantisera and six well-characterized monoclonal antibodies (MoAb) to study the HLA class II antigens on CALLA-positive malignant B cell populations and autologous normal B cell lines. Forty additional HLA class II-specific MoAb were also tested for their ability to bind to these cells. By using indirect immunofluorescence and immune precipitation assays, we find that malignant B cells often fail to express one or more of the three known types of HLA class II antigens. Cell lines with the following five phenotypes have been identified: HLA-DR+, -DQ+, -DP+; HLA-DR+, -DQ-, -DP+; HLA-DR-, -DQ+, -DP+; HLA-DR-, -DQ-, -DP+; and HLA-DR-, -DQ-, -DP-. These cell lines have been used to characterize the subregion specificity of MoAb that react with HLA class II antigens. This work confirms the existence of complicated patterns of serologic cross-reactivity between the three different types of HLA class II molecules. It also increases our understanding of the specificity of individual MoAb, thereby facilitating future investigation of the distribution and function of individual antigens. Our studies are consistent with the proposal that altered expression of HLA antigens on tumors might impair recognition of these cells by the immune system of the host, thereby contributing to the proliferation of a malignant clone.

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16

Dong, Rui-Ping, Akinori Kimura, Fujio Numano, Michiyoshi Yajima, Yuji Hashimoto, Yukio Kishi, Yasuharu Nishimura, and Takehiko Sasazuki. "HLA-DP antigen and Takayasu arteritis." Tissue Antigens 39, no. 3 (March 1992): 106–10. http://dx.doi.org/10.1111/j.1399-0039.1992.tb01918.x.

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17

Meyer, Christian G., Jürgen May, and Leonhard Schnittger. "HLA-DP — part of the concert." Immunology Today 18, no. 2 (February 1997): 58–61. http://dx.doi.org/10.1016/s0167-5699(96)30071-6.

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18

Gendzekhadze, Ketevan, Fidias Herrera, Silvia Montagnani, Omar Balbas, Klaus Witter, Ekkehard Albert, and Zulay Layrisse. "HLA-DP polymorphism in Venezuelan Amerindians." Human Immunology 65, no. 12 (December 2004): 1483–88. http://dx.doi.org/10.1016/j.humimm.2004.07.238.

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19

Middleton, D., D. Savage, J. Mytilneos, and G. Opelz. "HLA-DP matching in renal transplantation." Human Immunology 32 (October 1991): 87. http://dx.doi.org/10.1016/0198-8859(91)90277-g.

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20

Hutchlngs, C. J., M. C. Hillarby, M. J. Mcmahon, W. E. R. Ollier, and D. M. Grennan. "HLA-DPAI aND HLA-DPBl in Rheumatoid Arthritis And Its Subsets." Disease Markers 11, no. 1 (1993): 37–44. http://dx.doi.org/10.1155/1993/583825.

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The aim of this study was to examine the relationship between HLA-DP and susceptibility to articular and extra-articular features (Felty's syndrome and vasculitis) of rheumatoid arthritis (RA). The possible association of DP types with severity of articular disease was also analysed. No statistically significant associations were observed between HLA-DP alleles and articular or extra-articular features of RA, or to the severity of the arthritis when p was corrected for the number of alleles tested.

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Tsujisaki, M., M. Igarashi, K. Sakaguchi, M. Eisinger, M. Herlyn, and S. Ferrone. "Immunochemical and functional analysis of HLA class II antigens induced by recombinant immune interferon on normal epidermal melanocytes." Journal of Immunology 138, no. 4 (February 15, 1987): 1310–16. http://dx.doi.org/10.4049/jimmunol.138.4.1310.

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Abstract The effect of recombinant immune interferon (IFN-gamma) on the expression and shedding of HLA antigens and of melanoma-associated antigens (MAA) by epidermal melanocytes was investigated by using serologic and immunochemical techniques. IFN-gamma enhances the expression and/or shedding of HLA class I antigens and of the cytoplasmic MAA defined by monoclonal antibody (MoAb) 465.12S and induces a slight reduction in the expression of the high m.w. melanoma-associated antigen (HMW-MAA). In agreement with the data in the literature, melanocytes incubated with IFN-gamma acquire HLA-DR, -DQ, and -DP antigens. Contrary to previous information in the literature, the effect is not restricted to HLA class II antigens, since IFN-gamma also induces the expression of the 96-kDa MAA recognized by MoAb CL203. The effect of IFN-gamma on HLA class II antigens and 96-kDa MAA is dose and time dependent and is specific, because recombinant leukocyte interferon affects the expression of neither type of antigen. In spite of the expression of HLA class II antigens, IFN-gamma-treated melanocytes do not acquire the ability to stimulate the proliferation of allogeneic lymphocytes. HLA-DR antigens are more susceptible to induction by IFN-gamma than HLA-DQ and -DP antigens, since the percentage of melanocytes acquiring HLA-DQ and -DP antigens is lower than that acquiring HLA-DR antigens. Furthermore, the dose of IFN-gamma is higher and the time of incubation is longer to induce HLA-DQ and -DP antigens than to induce HLA-DR antigens. The differential susceptibility of HLA-DR, -DQ, and -DP antigens as well as of melanocytes from various donors to the modulating effect of IFN-gamma may provide an explanation for the more frequent detection of HLA-DR than of HLA-DQ and -DP antigens in melanoma lesions and for the expression of HLA class II antigens by some, but not all, melanoma lesions.

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Santamaria, P., NL Reinsmoen, AL Lindstrom, MT Boyce-Jacino, JJ Barbosa, AJ Faras, PB McGlave, and SS Rich. "Frequent HLA class I and DP sequence mismatches in serologically (HLA- A, HLA-B, HLA-DR) and molecularly (HLA-DRB1, HLA-DQA1, HLA-DQB1) HLA- identical unrelated bone marrow transplant pairs [published erratum appears in Blood 1994 Jun 15;83(12):3834]." Blood 83, no. 1 (January 1, 1994): 280–87. http://dx.doi.org/10.1182/blood.v83.1.280.280.

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Abstract The rates of graft-versus-host disease (GVHD) and rejection are significantly higher among recipients of unrelated donor marrow (BM) than in recipients of marrow from HLA-identical siblings, even when donors and recipients are mixed lymphocyte culture (MLC) compatible and serologically and Dw identical. It has been hypothesized that phenotypically silent HLA class I and DP sequence mismatches might be associated with these differences, but little is known about their incidence. We have sequenced the HLA-A, HLA-B, HLA-C, HLA-DPA1, and HLA- DPB1 genes expressed by 12 unrelated marrow transplant pairs, 11 of whom were molecularly matched at DRB, DQA1, and DQB1 loci. Nine of these pairs were also HLA-A and HLA-B matched by serology. Six of these nine “HLA-identical” pairs were HLA-A (2 of 6), HLA-B (1 of 6), and HLA- C (6 of 6) mismatched at the sequence level. The mismatched class I alleles of all these pairs had strikingly different sequence motifs in the six specificity pockets of their antigen recognition site, and in five pairs they also had sequence differences at positions implicated in T-cell receptor (TCR) binding. Two of the three pairs who were serologically mismatched for one HLA-A or HLA-B antigen were also sequence mismatched at HLA-C. Finally, 10 of 11 pairs tested expressed different DP sequences. These data indicate that HLA class I, especially HLA-C, and DP sequence mismatches are frequent among unrelated subjects defined as HLA identical by current typing methods. We speculate that these sequence differences may explain, at least in part, the higher incidence of acute GVHD and rejection in unrelated BM transplantation as opposed to transplantation between HLA-identical siblings. Because of their high frequency, the role of HLA-A, HLA-B, HLA-C, and HLA-DP mismatches in transplantation outcome is now amenable to direct study.

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Santamaria, P., NL Reinsmoen, AL Lindstrom, MT Boyce-Jacino, JJ Barbosa, AJ Faras, PB McGlave, and SS Rich. "Frequent HLA class I and DP sequence mismatches in serologically (HLA- A, HLA-B, HLA-DR) and molecularly (HLA-DRB1, HLA-DQA1, HLA-DQB1) HLA- identical unrelated bone marrow transplant pairs [published erratum appears in Blood 1994 Jun 15;83(12):3834]." Blood 83, no. 1 (January 1, 1994): 280–87. http://dx.doi.org/10.1182/blood.v83.1.280.bloodjournal831280.

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The rates of graft-versus-host disease (GVHD) and rejection are significantly higher among recipients of unrelated donor marrow (BM) than in recipients of marrow from HLA-identical siblings, even when donors and recipients are mixed lymphocyte culture (MLC) compatible and serologically and Dw identical. It has been hypothesized that phenotypically silent HLA class I and DP sequence mismatches might be associated with these differences, but little is known about their incidence. We have sequenced the HLA-A, HLA-B, HLA-C, HLA-DPA1, and HLA- DPB1 genes expressed by 12 unrelated marrow transplant pairs, 11 of whom were molecularly matched at DRB, DQA1, and DQB1 loci. Nine of these pairs were also HLA-A and HLA-B matched by serology. Six of these nine “HLA-identical” pairs were HLA-A (2 of 6), HLA-B (1 of 6), and HLA- C (6 of 6) mismatched at the sequence level. The mismatched class I alleles of all these pairs had strikingly different sequence motifs in the six specificity pockets of their antigen recognition site, and in five pairs they also had sequence differences at positions implicated in T-cell receptor (TCR) binding. Two of the three pairs who were serologically mismatched for one HLA-A or HLA-B antigen were also sequence mismatched at HLA-C. Finally, 10 of 11 pairs tested expressed different DP sequences. These data indicate that HLA class I, especially HLA-C, and DP sequence mismatches are frequent among unrelated subjects defined as HLA identical by current typing methods. We speculate that these sequence differences may explain, at least in part, the higher incidence of acute GVHD and rejection in unrelated BM transplantation as opposed to transplantation between HLA-identical siblings. Because of their high frequency, the role of HLA-A, HLA-B, HLA-C, and HLA-DP mismatches in transplantation outcome is now amenable to direct study.

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24

Fleischhauer, Katharina, and Bronwen E. Shaw. "HLA-DP in unrelated hematopoietic cell transplantation revisited: challenges and opportunities." Blood 130, no. 9 (August 31, 2017): 1089–96. http://dx.doi.org/10.1182/blood-2017-03-742346.

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Abstract When considering HLA-matched hematopoietic cell transplantation (HCT), sibling and unrelated donors (UDs) are biologically different because UD-HCT is typically performed across HLA-DP disparities absent in sibling HCT. Mismatched HLA-DP is targeted by direct alloreactive T cell responses with important implications for graft-versus-host disease and graft-versus-leukemia. This concise review details special features of HLA-DP as model antigens for clinically permissive mismatches mediating limited T-cell alloreactivity with minimal toxicity, and describes future avenues for their exploitation in cellular immunotherapy of malignant blood disorders.

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25

Klobuch, Sebastian, Kathrin Hammon, Sarah Vatter-Leising, Elisabeth Neidlinger, Michael Zwerger, Annika Wandel, Laura Maria Neuber, et al. "HLA-DPB1 Reactive T Cell Receptors for Adoptive Immunotherapy in Allogeneic Stem Cell Transplantation." Cells 9, no. 5 (May 20, 2020): 1264. http://dx.doi.org/10.3390/cells9051264.

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HLA-DPB1 antigens are mismatched in about 80% of allogeneic hematopoietic stem cell transplantations from HLA 10/10 matched unrelated donors and were shown to be associated with a decreased risk of leukemia relapse. We recently developed a reliable in vitro method to generate HLA-DPB1 mismatch-reactive CD4 T-cell clones from allogeneic donors. Here, we isolated HLA-DPB1 specific T cell receptors (TCR DP) and used them either as wild-type or genetically optimized receptors to analyze in detail the reactivity of transduced CD4 and CD8 T cells toward primary AML blasts. While both CD4 and CD8 T cells showed strong AML reactivity in vitro, only CD4 T cells were able to effectively eliminate leukemia blasts in AML engrafted NOD/SCID/IL2Rγc−/− (NSG) mice. Further analysis showed that optimized TCR DP and under some conditions wild-type TCR DP also mediated reactivity to non-hematopoietic cells like fibroblasts or tumor cell lines after HLA-DP upregulation. In conclusion, T cells engineered with selected allo-HLA-DPB1 specific TCRs might be powerful off-the-shelf reagents in allogeneic T-cell therapy of leukemia. However, because of frequent (common) cross-reactivity to non-hematopoietic cells with optimized TCR DP T cells, safety mechanisms are mandatory.

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26

Haryati, S., Y. Sari, A. APrasetyo, and R. Sariyatun. "HLA-DP, HLA-DQ, and HLA-DR-restricted epitopes in GRA5 oftoxoplasma gondiistrains." IOP Conference Series: Materials Science and Engineering 107 (February 5, 2016): 012052. http://dx.doi.org/10.1088/1757-899x/107/1/012052.

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27

Edwards, J. A., B. M. Durant, D. B. Jones, P. R. Evans, and J. L. Smith. "Differential expression of HLA class II antigens in fetal human spleen: relationship of HLA-DP, DQ, and DR to immunoglobulin expression." Journal of Immunology 137, no. 2 (July 15, 1986): 490–97. http://dx.doi.org/10.4049/jimmunol.137.2.490.

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Abstract Frozen sections of human fetal spleen from 12 to 20 wk gestation were examined by using polyclonal antibodies to Ig isotypes, monoclonal antibodies to HLA class II subregion locus products, B and T cells, and follicular dendritic cells. Scattered lymphoid cells in spleen sections from fetuses of 12 to 13 wk gestational age expressed IgM but not IgD. The appearance of lymphoid cells expressing IgD occurred at 14 to 15 wk before the formation of loose clusters of B cells at 16 wk. IgD expression was associated mainly with cells in these clusters, which by 17 wk had become definite follicles. Follicular dendritic cells were not detectable until 20 wk. OKT3-positive T cells were not detected until 17 wk, and at 20 wk constituted 5% of the nucleated cell population. HLA-DR- and DP-positive lymphocytes and macrophages were detectable in fetal spleen from 12 wk onward; DR was expressed on more cells than DP, and the numbers of cells stained by HLA-DR-specific monoclonal antibodies exceeded the number of Ig-positive cells in all spleens examined. HLA-DQ was expressed by consistently fewer cells than HLA-DR and -DP in all spleens tested. The small number of DQ-positive cells in spleens from 12- to 13-wk fetuses had the morphology of macrophages; HLA-DQ expression by lymphoid cells followed a similar pattern to IgD expression and was associated mainly with follicular lymphocytes. It could be demonstrated by double-labeling experiments that all follicular IgM-positive cells in 17- to 20-wk spleens expressed HLA-DP, DQ, and DR antigens: IgM-positive cells in 12- to 16-wk spleens and interfollicular IgM-positive cells in 17- to 20-wk spleens all expressed HLA-DR, but only 59% and 43% expressed DP and DQ, respectively. Ninety-one to 100% of IgD-positive cells in all spleens examined expressed HLA-DQ in addition to DR and DP. In these experiments IgD-negative, DQ-positive cells had the morphologic appearance characteristic of macrophages. These data suggest that class II antigens are differentially expressed on developing lymphoid cells; DR and DP expression occurring in the earliest spleens examined, with expression of DP on a subpopulation of DR-positive cells; IgD and DQ expression appears to be coincident on maturing B cells as they begin to form follicles. An immunoregulatory role for HLA-DQ in B cell development is implicated and remains to be fully investigated.

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28

Rodriguez de Cordoba, S., P. Marshall, and P. Rubinstein. "Molecular characterization by high resolution isoelectric focusing of the products encoded by the class II region loci of the MHC in humans. II. DP alpha and DP beta gene variants." Journal of Immunology 142, no. 3 (February 1, 1989): 836–41. http://dx.doi.org/10.4049/jimmunol.142.3.836.

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Abstract To characterize the molecular polymorphism of the DP alpha and DP beta gene products, the HLA-DP molecules expressed by more than 200 cell lines were individually immunoprecipitated by using the mAb B7/21 and their neuraminidase-treated DP alpha and DP beta chains analyzed in IEF gels. These cell lines, most of them from members of 32 families, allowed the definition, by segregation analysis, of the IEF patterns of the DP polypeptide chains encoded by 129 distinct haplotypes. Both DP alpha and DP beta chains display polymorphic IEF-banding patterns. Two DP alpha (A and B) and seven DP beta (A, B, C, D, E, F, and G) IEF variants were characterized. The DP alpha B variant was found in linkage disequilibrium with both DP beta B and DP beta D. Linkage disequilibrium was also encountered with alleles at the DR and DQ loci. Finally, the correlations between the IEF DP alpha and DP beta variants and the primed lymphocyte test-defined HLA-DP specificities were determined by using a panel of 24 primed lymphocyte test-typed cell lines.

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29

Haan, Keith M., William W. Kwok, Richard Longnecker, and Peter Speck. "Epstein-Barr Virus Entry Utilizing HLA-DP or HLA-DQ as a Coreceptor." Journal of Virology 74, no. 5 (March 1, 2000): 2451–54. http://dx.doi.org/10.1128/jvi.74.5.2451-2454.2000.

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ABSTRACT Epstein-Barr virus (EBV) glycoprotein gp350/gp220 association with cellular CD21 facilitates virion attachment to B lymphocytes. Membrane fusion requires the additional interaction between virion gp42 and cellular HLA-DR. This binding is thought to catalyze membrane fusion through a further association with the gp85-gp25 (gH-gL) complex. Cell lines expressing CD21 but lacking expression of HLA class II molecules are resistant to infection by a recombinant EBV expressing enhanced green fluorescent protein. Surface expression of HLA-DR, HLA-DP, or HLA-DQ confers susceptibility to EBV infection on resistant cells that express CD21. Therefore, HLA-DP or HLA-DQ can substitute for HLA-DR and serve as a coreceptor in EBV entry.

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30

Bodmer, JuliaG, Susan Tonks, AmitM Oza, T. Andrew Lister, and WalterF Bodmer. "HLA-DP BASED RESISTANCE TO HODGKIN'S DISEASE." Lancet 333, no. 8652 (June 1989): 1455–56. http://dx.doi.org/10.1016/s0140-6736(89)90166-9.

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Marshall, William H., Sheila Drover, Dianne Codner, Jane Gamberg, M. Douglas Copp, Hong-Wei Liu, Lang-Tuo Deng, and H. Banfield Younghusband. "HLA-DP Epitope Typing Using Monoclonal Antibodies." Human Immunology 59, no. 3 (March 1998): 189–97. http://dx.doi.org/10.1016/s0198-8859(98)00003-2.

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32

Lupita, Geer, and Park Min Sik. "Recognition of conformational epitopes of HLA-DP." Human Immunology 47, no. 1-2 (April 1996): 102. http://dx.doi.org/10.1016/0198-8859(96)85251-7.

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Daniel, Cook, Roeske Larissa, Goldfarb David, Dennis Vincent, Koo Anna, and Hodge Ernest. "Is HLA-DP a kidney transplantation antigen?" Human Immunology 47, no. 1-2 (April 1996): 131. http://dx.doi.org/10.1016/0198-8859(96)85411-5.

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Lee, Janet S., Silvia Sartoris, Paola Briata, Ed Choi, Constance Cullen, Denis Lepaslier, and Ivan Yunis. "Sequence polymorphism of HLA-DP beta chains." Immunogenetics 29, no. 5 (May 1989): 346–49. http://dx.doi.org/10.1007/bf00352845.

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35

Sell, Thomas W., and David D. Eckels. "Primary mixed lymphocyte responses to HLA-DP." Human Immunology 29, no. 1 (September 1990): 23–30. http://dx.doi.org/10.1016/0198-8859(90)90066-x.

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Müller, C. A., G. Bitzer, S. Fenchel, G. Ehninger, and H. Schmidt. "HLA-DP matching in bone marrow transplantation." Human Immunology 36, no. 1 (January 1993): 62. http://dx.doi.org/10.1016/0198-8859(93)90087-h.

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37

Douhan, John, Rebecca Lieberson, Joan H. M. Knoll, Hong Zhou, and Laurie H. Glimcher. "An Isotype-specific Activator of Major Histocompatibility Complex (MHC) Class II Genes That Is Independent of Class II Transactivator." Journal of Experimental Medicine 185, no. 11 (June 2, 1997): 1885–95. http://dx.doi.org/10.1084/jem.185.11.1885.

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Patients with one type of major histocompatibility complex class II combined immunodeficiency have mutations in a gene termed class II transactivator (CIITA), which coordinately controls the transcription of the three major human class II genes, HLA-DR, -DQ, and -DP. However, the experimentally derived B-lymphoblastoid cell line, clone 13, expresses high levels of HLADQ in the absence of HLA-DR and HLA-DP, despite its mapping by complementation analysis to this group. It was possible that one of the clone 13 CIITA alleles bore a mutation that allowed HLA-DQ, but not HLA-DR or -DP transcription. Alternatively, another factor, distinct from CIITA, might control HLA-DQ expression. We report here that ectopic expression of CIITA cDNAs derived by reverse transcriptase polymerase chain reaction from clone 13 do not restore expression of HLA-DQ in another CIITA-deficient cell line, RJ2.2.5. In addition, no CIITA protein is detectable in clone 13 nuclear extracts. In contrast, somatic cell fusion between clone 13 and RJ2.2.5 restored expression of the HLA-DQ haplotype encoded by the RJ2.2.5 DQB gene. Taken together, these data demonstrate the existence of an HLA-DQ isotype-specific trans-acting factor, which functions independently of CIITA.

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van Lith, Marcel, Rosanna M. McEwen-Smith, and Adam M. Benham. "HLA-DP, HLA-DQ, and HLA-DR Have Different Requirements for Invariant Chain and HLA-DM." Journal of Biological Chemistry 285, no. 52 (October 19, 2010): 40800–40808. http://dx.doi.org/10.1074/jbc.m110.148155.

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39

Gonwa, T. A., J. P. Frost, and R. W. Karr. "All human monocytes have the capability of expressing HLA-DQ and HLA-DP molecules upon stimulation with interferon-gamma." Journal of Immunology 137, no. 2 (July 15, 1986): 519–24. http://dx.doi.org/10.4049/jimmunol.137.2.519.

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Abstract We have simultaneously studied expression of all three classes of human Ia (HLA-DR, DP, and DQ) on normal human B cells and monocytes (M phi) by using two-color immunofluorescence and flow cytometry. Expression was investigated on freshly isolated cells and after incubation of cells for 48 and 96 hr in interferon-gamma (IFN-gamma). All freshly isolated B cells express high levels of DR, DQ, and DP, and these levels are unchanged by incubation with IFN-gamma for 48 hr and 96 hr. In contrast, freshly isolated M phi are on the average 91% DR+, 32% DQ+, and 15% DP+. Incubation with IFN-gamma increases Ia expression on M phi to 98% DR+, 75% DQ+, and 58% DP+ at 48 hr, with virtually all cells becoming positive for all three Ia antigens at 96 hr. Furthermore, after the 96-hr incubation, antigen density increases 10-fold for DR, 15-fold for DQ, and 15-fold for DP in M phi to reach levels of expression comparable with B cells. These studies demonstrate that all peripheral blood monocytes have the capacity to become HLA-DQ and HLA-DP positive; IFN-gamma regulates expression of all three classes of human Ia in M phi; and IFN-gamma does not significantly modulate Ia expression in B cells.

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40

Baas, E. J., R. E. Bontrop, N. Otting, and M. J. Giphart. "Molecular analysis of HLA-DP specificities HLA-DPw1, -DPw2 and -DPw4: DP beta chain heterogeneity correlates with PLT subtyping." Tissue Antigens 31, no. 1 (January 1988): 5–13. http://dx.doi.org/10.1111/j.1399-0039.1988.tb02059.x.

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41

Tanigaki, Nobuyuki, Roberto Tosi, Barbara Parodi, Rosa Sorrentino, Giovanni B. Ferrara, and Jack L. Strominger. "Detection of HLA-DP serological allodeterminants by the use of radioiodinated DP molecules." European Journal of Immunology 17, no. 6 (1987): 743–50. http://dx.doi.org/10.1002/eji.1830170602.

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Solomon, Scott R., Michael T. Aubrey, Xu Zhang, Katelin C. Jackson, Lawrence E. Morris, H. Kent Holland, Melhem M. Solh, and Asad Bashey. "Class II HLA mismatch improves outcomes following haploidentical transplantation with posttransplant cyclophosphamide." Blood Advances 4, no. 20 (October 27, 2020): 5311–21. http://dx.doi.org/10.1182/bloodadvances.2020003110.

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Abstract HLA disparity is the major predictor of outcome following unrelated donor (UD) transplantation, where a single mismatch (mm) at the HLA-A, HLA-B, HLA-C, or HLA-DRB1 locus leads to increased mortality, and mismatching at multiple loci compounds this effect. In contrast, HLA disparity has not been shown to increase mortality in the context of haploidentical transplant using posttransplant cyclophosphamide (PTCy). To better define the consequences of loci-specific HLA mm, we analyzed 208 consecutive patients undergoing haploidentical transplantation for hematologic malignancy using PTCy at our institution (median age, 52 years [range, 19-75 years]; peripheral blood stem cell, 66%; reduced-intensity conditioning, 59%). Median follow-up was 65.4 months (range, 34.3-157.2 months). In univariate analysis, a single class II HLA mm at HLA-DR, HLA-DQ or a nonpermissive (np) HLA-DP mm had a protective effect on disease-free and overall survival (OS), primarily a result of reduced relapse risk. Furthermore, this survival effect was cumulative, so that patients with 3 class II mm (HLA-DR, HLA-DQ, and np HLA-DP) had the best OS. In multivariate analysis, HLA-DR mm and np HLA-DP mm were both independently associated with improved OS (hazard ratio [HR], 0.43; P =.001; and HR, 0.47; P =.011, respectively). In contrast, single or multiple mm at HLA-A, HLA-B, or HLA-C loci had no effect on acute graft-versus-host disease (GVHD), nonrelapse mortality (NRM), relapse, or survival, although the presence of an HLA-A mm was associated with increased chronic GVHD incidence. The association of class II mm with lower relapse occurred without a corresponding increase in NRM or acute or chronic GVHD. These findings will require validation in larger registry studies.

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Gerrard, T. L., D. R. Dyer, and H. S. Mostowski. "IL-4 and granulocyte-macrophage colony-stimulating factor selectively increase HLA-DR and HLA-DP antigens but not HLA-DQ antigens on human monocytes." Journal of Immunology 144, no. 12 (June 15, 1990): 4670–74. http://dx.doi.org/10.4049/jimmunol.144.12.4670.

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Abstract A number of cytokines were tested for their ability to modulate HLA-DR Ag expression on normal human monocytes. IL-4, granulocyte-macrophage (GM)-CSF as well as IFN-gamma were able to increase HLA-DR Ag expression on monocytes. IFN-alpha was also able to augment HLA-DR Ag expression, but to a lesser degree. Macrophage-CSF, granulocyte-CSF, TNF-alpha, TNF-beta, and IL-6 were not able to augment HLA-DR Ag expression. There were distinct patterns in the ability of different cytokines to augment class II histocompatibility Ag expression. IL-4 and GM-CSF selectively increased only HLA-DR and HLA-DP, but did not increase HLA-DQ antigens on monocytes. IFN-gamma, however, was able to augment the expression of HLA-DR, HLA-DP, and HLA-DQ Ag. Combinations of IFN-gamma with either IL-4 or GM-CSF did not show any synergy for the augmentation of any of the class II antigens on monocytes.

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Islam, S. M. Shamsul, Hyoun-Ah Kim, Bunsoon Choi, Ju-Yang Jung, Sung-Min Lee, Chang-Hee Suh, and Seonghyang Sohn. "Differences in Expression of Human Leukocyte Antigen Class II Subtypes and T Cell Subsets in Behçet’s Disease with Arthritis." International Journal of Molecular Sciences 20, no. 20 (October 11, 2019): 5044. http://dx.doi.org/10.3390/ijms20205044.

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It has been reported Human Leukocyte Antigen (HLA) gene polymorphism is a risk factor for the development of Behçet’s disease (BD). In this study, the association of HLA class II subtypes HLA-DP, DQ, DR, and T cell subsets in BD patients with arthritis was evaluated. Frequencies of HLA-DP, DQ, DR positive cells, and T cell subsets in peripheral blood leukocytes (PBL) were measured by flow cytometric analysis in BD, and compared to rheumatoid arthritis as disease controls and healthy controls. Frequencies of HLA-DQ were significantly decreased in whole PBL and granulocytes of BD active patients as compared to healthy controls. In monocytes populations, proportions of HLA-DR positive cells were significantly increased in BD active patients as compared to healthy controls. Proportions of CD4+CCR7+ and CD8+CCR7+ cells were significantly higher in BD active patients than in BD inactive in whole PBL. Frequencies of CD4+CD62L- and CD8+CD62L- cells in lymphocytes were significantly decreased in active BD than those in inactive BD. There were also correlations between disease activity markers and T cell subsets. Our results revealed HLA-DP, DQ, and DR expressing cell frequencies and several T cell subsets were significantly correlated with BD arthritis symptoms.

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Fleischhauer, Katharina, Elisabetta Zino, Benedetta Mazzi, Elisabetta Sironi, Paolo Servida, Elisabetta Zappone, Elena Benazzi, and Claudio Bordignon. "Peripheral blood stem cell allograft rejection mediated by CD4+ T lymphocytes recognizing a single mismatch at HLA-DPβ1*0901." Blood 98, no. 4 (August 15, 2001): 1122–26. http://dx.doi.org/10.1182/blood.v98.4.1122.

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Little is known about the molecular characteristics of alloantigens recognized by alloreactive T cells mediating hematologic stem cell graft rejection. In particular, it has never been shown that such alloantigens can be encoded by HLA-DPβ alleles. Indeed, matching for HLA-DP antigens is generally not considered to be of functional importance for the outcome of allogeneic bone marrow or peripheral blood stem cell transplantation. In this study, a case of peripheral blood stem cell allograft rejection was investigated in which the patient and donor differed for a single mismatch at HLA-DP in the rejection direction. Patient-derived T lymphocytes circulating at the time of rejection showed direct ex vivo cytotoxic activity against donor-derived B-lymphoblastoid cells as well as other HLA-DPβ1*0901–expressing targets. The presence of HLA-DPβ1*0901–specific effectors in vivo was further confirmed by in vitro stimulation experiments. CD4+ T-cell lines and clones with specific cytotoxic activity against HLA-DPβ1*0901–expressing targets including donor B-lymphoblastoid cells were generated both by nonspecific and by donor-specific in vitro stimulation. Taken together, these data demonstrate that HLA-DP can be the target antigen of cytotoxic CD4+ T lymphocytes involved in peripheral blood stem cell allograft rejection.

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Pious, D., L. Dixon, F. Levine, T. Cotner, and R. Johnson. "HLA class II regulation and structure. Analysis with HLA-DR3 and HLA-DP point mutants." Journal of Experimental Medicine 162, no. 4 (October 1, 1985): 1193–207. http://dx.doi.org/10.1084/jem.162.4.1193.

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Point mutations that affect HLA-DR structure or expression have not previously been described. In the present study, we isolated such mutants by immunoselection of an ethyl methanesulfonate-mutagenized HLA-DR3 cell line with an anti-HLA-DR3 monoclonal antibody, 16.23. To facilitate analysis, we used a parent cell line with a preexisting deletion of one haplotype encompassing DR and DQ alpha and beta. The selection yielded two sets of mutants, one with defects in DR3 structure, the other with defects in different steps leading to DR expression. Of the expression-defective mutants, one had undergone a second deletion removing the remaining DR alpha gene but no other class II genes. It had a normal abundance of DR beta mRNA but had lost binding of DR monomorphic antibodies, indicating that DR beta chains do not form noncognate dimers. A second mutant had an abnormally large DR alpha mRNA, probably resulting from a splice site mutation. Several mutants had marked reductions in DR beta mRNA levels; in two of these, the lesion appeared to be transcriptional because the reduction in DR beta mRNA was paralleled by an altered methylation pattern of one of the DR beta genes. Other expression-defective mutants had different posttranscriptional defects. Some of the mutations were similar to those that have been found in mouse strains defective in I-E expression, whereas others have no known natural counterpart. The matrix of reactivities of anti-HLA class II monomorphic antibodies with these and similar mutants allowed us to define the gene products recognized by these antibodies. A set of seven mutants were "epitope defective," that is, they expressed normal or near normal levels of HLA-DR3 but no longer bound 16.23. Unexpectedly, each of the epitope mutants had decreased DR dimer stability. These mutants should be useful in localizing the DR3 alloepitope and in elucidating its contribution as a restriction element in the presentation of soluble antigen to immune T cells.

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BAISCH, J. M., and J. D. CAPRA. "Linkage Disequilibrium within the HLA Complex does not extend into HLA-DP." Scandinavian Journal of Immunology 37, no. 4 (April 1993): 499–503. http://dx.doi.org/10.1111/j.1365-3083.1993.tb03325.x.

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Ling, Min, Kwaku Marfo, Peter Masiakos, Aws Aljanabi, Joel Lindower, Daniel Glicklich, Graciela de Boccardo, et al. "Pretransplant anti-HLA-Cw and anti-HLA-DP antibodies in sensitized patients." Human Immunology 73, no. 9 (September 2012): 879–83. http://dx.doi.org/10.1016/j.humimm.2012.07.320.

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Bray, Robert, Sandy Rosen-Bronson, Michael Haagenson, John Klein, Susan Flesch, Cynthia Vierra-Green, Stephen Spellman, and Claudio Anasetti. "The Detection of Donor-Directed, HLA-Specific Alloantibodies in Recipients of Unrelated Hematopoietic Cell Transplantation Is Predictive of Graft Failure." Blood 110, no. 11 (November 16, 2007): 475. http://dx.doi.org/10.1182/blood.v110.11.475.475.

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Abstract:

Abstract Animal studies point to a strong role for MHC-specific antibody as a cause for failed donor hematopoietic cell engraftment, but the role of donor-directed HLA-specific allo-antibodies in human transplants has been controversial. To investigate such a role, we used a retrospective case-control design and studied unrelated donor:recipient pairs whose transplants were facilitated through the NMDP. A total of 37 cases with graft failure and 78 matched control pairs were evaluated. The 37 graft failure cases were selected based on survival beyond 28 days of transplant with no sustained engraftment, and available cryopreserved recipient serum to test for HLA-specific alloantibodies. Up to 3 controls were selected for each case, and matched for disease, disease status, graft type, patient age and year of transplant. Patients had AML, ALL, CML or MDS, 98% received myeloablative conditioning regimens, 100% received T replete grafts, 97% received marrow, and 97% received calcineurin-based GVHD prophylaxis. Patients and donors were retrospectively typed for HLA-A,B,Cw,DRB1,DQB1,DQA1,DPB1,and DPA1 by sequencing or other high resolution typing methods. Stored pre-transplant serum samples (patients and controls) were retrieved from the NMDP Research Repository, and assayed for HLA antibodies by solid-phase FlowPRA (One Lambda, Inc). All positive samples were evaluated for HLA specificity by single-antigen microparticles (LabScreen, One Lambda, Inc). Among the 37 failed transplants, 11 (30%) recipients possessed alloantibodies specific for donor HLA Class I or Class II, compared to only 3 (4%) of 78 controls. HLA-DR or DQ specific antibodies were not detected; hence, all HLA Class II-specific antibodies were directed to DP. Recipients with anti-DP antibodies against the donor mismatched DP were at increased risk of graft failure, indicating the importance of recipient antibodies directed against mismatched donor DP antigens. Exact conditional logistic regression analysis for the presence of either Class I HLA-A,B,Cw or Class II HLA-DP antibodies showed similar findings (Class I alone: OR. 6.31: 95% CI 1.17–62.9; p=0.03, Class II alone: OR 12.00; 95% CI 1.46–551.97; p=0.01, Class I and II combined: OR 19.08; 95% CI 2.72–828.49; p=0.0003). Further analyses were conducted to evaluate a limited set of covariates not accounted for in the case:control study, i.e. patient CMV status, cell dose and HLA-C match. Cell dose and CMV status were independently predictive of engraftment, p=0.01 and 0.03, respectively. No effect was observed for HLA-Cw match (p=0.84). The presence of anti-donor HLA Class I or II antibodies was predictive of engraftment when adjustment was made for either cell dose (OR 15.49; 95% CI 2.06–697.83; p=0.002) or CMV status (OR 7.94; 95% CI 0.97–367.84; p=0.05). In summary, these results indicate that donor-specific HLA Class I or Class II antibodies in recipients of unrelated donor hematopoietic cell transplants are associated with failed engraftment. We recommend that, as a “Standard-of-Practice”, all potential recipients be screened for the presence of HLA class I and class II antibodies including HLA DP. Donors should be excluded if they carry mismatched HLA types against which the patient has specific antibodies.

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May, J., P. G. Kremsner, L. Schnittger, C. G. Meyer, U. Bienzle, D. Milovanovic, and C. C. Löliger. "HLA-DP control of human Schistosoma haematobium infection." American Journal of Tropical Medicine and Hygiene 59, no. 2 (August 1, 1998): 302–6. http://dx.doi.org/10.4269/ajtmh.1998.59.302.

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