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Journal articles on the topic 'Allospecificity'

Author: Grafiati

Published: 9 March 2023

Last updated: 10 March 2023

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1

TRABACE, S., M. C. MAZZILLI, I. CASCINO, P. LULLI, S. COSTANZI PORRINI, and E. GANDINI. "A mouse monoclonal antibody detecting the allospecificity HLA-A3." Tissue Antigens 23, no. 1 (December 11, 2008): 12–16. http://dx.doi.org/10.1111/j.1399-0039.1984.tb00002.x.

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2

Takahashi, Toshitada, Yasue Matsudaira, Yuichi Obatal, and Kazuo Moriwaki. "An autoreactive H-2-specific monoclonal antibody with allospecificity." Immunogenetics 26, no. 1-2 (1987): 105–6. http://dx.doi.org/10.1007/bf00345462.

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3

Zheng, W. P., K. Kiura, V. K. Milisauskas, E. DeNardin, and I. Nakamura. "Murine NK cell allospecificity-1 is defined by inhibitory ligands." Journal of Immunology 156, no. 12 (June 15, 1996): 4651–55. http://dx.doi.org/10.4049/jimmunol.156.12.4651.

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Abstract Hemopoietic allografts of normal and neoplastic origin are subject to NK cell-mediated resistance in mice. Susceptibility to this resistance is controlled by MHC-linked genes in a recessive manner. Several distinct specificities could be postulated to explain the strain-dependent pattern of resistance. These presumptive specificities for recognition are H-2 haplotype dependent, but the correspondence is not one-to-one. For example, resistance of H-2d or H-2b/d host to H-2 b graft operationally defines specificity-1, establishing its link with haplotype H-2b. To examine the molecular basis of specificity-1, spontaneous Dd-loss mutant clones were isolated from H-2b/d and H-2d hemopoietic cell lines, i.e., 416B of (C57BL/6 x DBA/2)F1 (B6D2F1) origin and L1210 of DBA/2 origin, both of which lack specificity-1. The expression of specificity-1 in the mutant clones was examined in vivo and in vitro. The results indicate that Dd-loss clones of 416B and L1210 lines express specificity-1. These data suggest that murine NK cell allospecificity-1 is defined primarily by the absence of the Dd molecule or other class I molecules sharing the protective motifs; no H-2b-associated genes play a relevant role. This conclusion is consistent with the missing self hypothesis of NK cell reactivity, and is in agreement with the observation that lysis of B6 targets by B6D2F1 NK cells is mediated mostly by cells that express Ly-49A and/or Ly-49G2.

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4

Zeevi, Adriana, John Fung, Tony R. Zerbe, Christina Kaufman, Bruce S. Rabin, Bartley P. Griffith, Robert L. Hardesty, and Rene J. Duquesnoy. "ALLOSPECIFICITY OF ACTIVATED T CELLS GROWN FROM ENDOMYOCARDIAL BIOPSIES FROM HEART TRANSPLANT PATIENTS." Transplantation 41, no. 5 (May 1986): 620–25. http://dx.doi.org/10.1097/00007890-198605000-00014.

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5

Pellegrino, M. A., P. Richiardi, and S. Ferrone. "8th International Histocompatibility Workshop Analysis of a goat antiserum to HLA-B15 allospecificity." Tissue Antigens 17, no. 5 (December 11, 2008): 542–45. http://dx.doi.org/10.1111/j.1399-0039.1981.tb00743.x.

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6

Liu, W., X. Xiao, C. Wu, and X. Li. "Allospecificity and Cytotoxicity of Innate Macrophages: Novel Role for Macrophages in Transplant Rejection?" Transplantation 98 (July 2014): 46. http://dx.doi.org/10.1097/00007890-201407151-00155.

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7

Matsuyama, T., J. Schwenzer, J. Silver, and R. Winchester. "Structural relationships between the DR beta 1 and DR beta 2 subunits in DR4, 7, and w9 haplotypes and the DRw53 (MT3) specificity." Journal of Immunology 137, no. 3 (August 1, 1986): 934–40. http://dx.doi.org/10.4049/jimmunol.137.3.934.

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Abstract The class II molecules of DR4, DR7, and DRw9 haplotypes were analyzed by immunoprecipitation, followed by two-dimensional gel electrophoresis and N-terminal amino acid sequencing. By using HLA-DR chain-specific monoclonal antibodies, two distinct DR beta-chains were identified. One beta-chain, designated DR beta 2, had a characteristic acidic mobility. In all three DR types the DR beta 2-chains were indistinguishable by two-dimensional gel electrophoresis and partial N-terminal sequencing. A second DR beta-chain designated beta 1 had a more basic mobility on two-dimensional gel electrophoresis, and differed from the DR beta 2-chains by the consistent presence of phenylalanine at position 18. In contrast to the DR beta 2-chains, the DR beta 1-chains were clearly polymorphic, with specific amino acid sequence differences characteristic of each DR type. The monoclonal antibodies 109d6 and 17-3-3S, recognizing distinct polymorphic epitopes similarly correlated with the DRw53 allospecificity, were found to react with different DR beta-chains. The epitope recognized by monoclonal antibody 109d6 was identified on the DR beta 2-chain in the prototypic DR4, DR7, and DRw9 cell lines. However, the DR7, Dw11, DQw3 cell line BEI was unreactive with antibody 109d6 by either immunofluorescence or immunoprecipitation despite the presence of the DRw53 allodeterminant on this cell line. The other DRw53-like monoclonal antibody, 17-3-3S, reacted with the DR beta 1-rather than the DR beta 2-chain in all DR4 and DR7 cell lines tested, including the cell line BEI. However, antibody 17-3-3S did not react with the DRw53-positive DRw9 cell line ISK. These studies suggest that the DRw53 allospecificity is more complex than previously thought and may comprise a number of distinct epitopes encoded by two different DR beta loci.

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8

Tokita, Daisuke, Masayuki Shishida, Hideki Ohdan, Takashi Onoe, Hidetaka Hara, Yuka Tanaka, Kohei Ishiyama, et al. "Liver Sinusoidal Endothelial Cells That Endocytose Allogeneic Cells Suppress T Cells with Indirect Allospecificity." Journal of Immunology 177, no. 6 (September 1, 2006): 3615–24. http://dx.doi.org/10.4049/jimmunol.177.6.3615.

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9

Callaghan, Chris J., Foad J. Rouhani, Margaret C. Negus, Allison J. Curry, Eleanor M. Bolton, J. Andrew Bradley, and Gavin J. Pettigrew. "Abrogation of Antibody-Mediated Allograft Rejection by Regulatory CD4 T Cells with Indirect Allospecificity." Journal of Immunology 178, no. 4 (February 2, 2007): 2221–28. http://dx.doi.org/10.4049/jimmunol.178.4.2221.

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10

Tapirdamaz, O., S. Mancham, L. V. D. Laan, G. Kazemier, K. Thielemans, H. J. Metselaar, and J. Kwekkeboom. "DETAILED KINETICS OF T-CELLS WITH DIRECT ALLOSPECIFICITY AFTER LIVER TRANSPLANTATION: A NOVEL ASSAY." Transplantation Journal 90 (July 2010): 237. http://dx.doi.org/10.1097/00007890-201007272-00450.

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11

Tsang, Julia, Shuiping Jiang, Yakup Tanriver, Eva Leung, Giovanna Lombardi, and Robert I. Lechler. "In-vitro generation and characterisation of murine CD4+CD25+ regulatory T cells with indirect allospecificity." International Immunopharmacology 6, no. 13-14 (December 2006): 1883–88. http://dx.doi.org/10.1016/j.intimp.2006.07.032.

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12

RODRÍGUEZ-SÁNCHEZ, EDNA, LAURA J. GIRALDO-KALIL, DONALD L. J. QUICKE, and ALEJANDRO ZALDÍVAR-RIVERÓN. "Two new species of the braconid wasp genus Bracon (Braconinae) from Los Tuxtlas region in Veracruz, Mexico, reared from fruits of three species of Lauraceae." Zootaxa 5162, no. 1 (July 5, 2022): 67–77. http://dx.doi.org/10.11646/zootaxa.5162.1.4.

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Two new species belonging to the braconid genus Bracon (Braconinae) are described from the tropical rainforest of Los Tuxtlas in the state of Veracruz, Mexico, B. laurae sp. nov. and B. rosamondae sp. nov. These species are morphologically similar and were reared from fruits of three Lauraceae species, Damburneya ambigens, D. salicifolia and Nectandra turbacensis. However, comparison of their DNA barcoding locus and a fragment of the nuclear ribosomal 28S gene confirmed their allospecificity. These two species share a number of morphological features with the two described Neotropical Bracon species that are known to be phytophagous (seed predators), B. phytophagus Quicke and B. zuleideae Perioto & Lara. We therefore propose a new species-group for the above four species, the B. phytophagus Quicke species-group, and suggest that the two newly described species also have a phytophagous feeding strategy.

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13

Tsang, Julia Yuen-Shan, Yakup Tanriver, Shuiping Jiang, Shao-An Xue, Kulachelvy Ratnasothy, Daxin Chen, Hans J. Stauss, R. Pat Bucy, Giovanna Lombardi, and Robert Lechler. "Conferring indirect allospecificity on CD4+CD25+ Tregs by TCR gene transfer favors transplantation tolerance in mice." Journal of Clinical Investigation 118, no. 11 (November 3, 2008): 3619–28. http://dx.doi.org/10.1172/jci33185.

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14

&NA;. "LIVER SINUSOIDAL ENDOTHELIAL CELLS CAPTURING ALLOGENEIC CELLS EXERT IMMUNOSUPPRESSIVE EFFECTS ON T CELLS WITH INDIRECT ALLOSPECIFICITY." Transplantation 82, Suppl 2 (July 2006): 126. http://dx.doi.org/10.1097/00007890-200607152-00176.

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15

Lauzurica, P., R. Bragado, D. López, B. Galocha, and J. A. López de Castro. "Asymmetric selection of T cell antigen receptor alpha- and beta-chains in HLA-B27 alloreactivity." Journal of Immunology 148, no. 11 (June 1, 1992): 3624–30. http://dx.doi.org/10.4049/jimmunol.148.11.3624.

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Abstract Endogenous peptides constitutively bind to class I MHC Ag and are thought to be integral parts of allospecific T cell epitopes. However, allospecific TCR can recognize structural features of the alloantigen as foreign. To define some crucial parameters determining HLA-B27 allorecognition, the structure of TCR alpha- and beta-chains from HLA-B27-specific CTL was analyzed. A strategy, based on V alpha and V beta family-specific oligonucleotides, was used for specific amplification and direct sequencing of TCR-alpha and -beta cDNA. We observed nonrandom usage of V beta segments and recurrent structural motifs within beta-chain junctional regions. In contrast, no structural restrictions were apparent among alpha-chains, even from CTL clones of related fine specificity. These results indicate an asymmetric contribution of TCR alpha- and beta-chains to HLA-B27 allospecificity among the CTL clones analyzed. They suggest recognition of multiple peptides and involvement of beta-chain junctional regions in recognizing shared motifs among some of these peptides.

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16

Wadgymar, Arturo, and Philip F. Halloran. "CROSSREACTIONS BETWEEN AN I-A ALLOSPECIFICITY AND THE CYTOSKELETON OF GLOMERULAR EPITHELIUM AND OF VASCULAR SMOOTH MUSCLE1." Transplantation 43, no. 6 (June 1987): 903–8. http://dx.doi.org/10.1097/00007890-198706000-00026.

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17

Wadgymar, Arturo, and Philip F. Halloran. "CROSSREACTIONS BETWEEN AN I-A ALLOSPECIFICITY AND THE CYTOSKELETON OF GLOMERULAR EPITHELIUM AND OF VASCULAR SMOOTH MUSCLE1." Transplantation 43, no. 6 (June 1987): 903–8. http://dx.doi.org/10.1097/00007890-198743060-00026.

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18

Choo, S. Y., L. A. Fan, and J. A. Hansen. "A novel HLA-B27 allele maps B27 allospecificity to the region around position 70 in the alpha 1 domain." Journal of Immunology 147, no. 1 (July 1, 1991): 174–80. http://dx.doi.org/10.4049/jimmunol.147.1.174.

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Abstract There are six known HLA-B alleles that share the HLA-B27 allospecificity, yet differ by one to six amino acid substitutions. Each of these B27 alleles can be readily assigned by one of the six representative IEF patterns. Two unrelated individuals, LH and HS, express B27 Ag that appear to be identical by IEF, but an HLA-B27 alloreactive CTL clone I-73 was found to react differently with these cells, suggesting these B27 molecules are not identical. We sequenced polymerase chain reaction-amplified B27 cDNA clones obtained from HS and compared its deduced amino acid sequence (B27-HS) with the B27 sequence of LH (B27-LH) which was previously designated the B*2701 allele. B27-HS and B27-LH differ by eight amino acids; three in alpha 1 domain and five in alpha 2 domain. These amino acid substitutions of B27-HS altered T cell recognition but not the B27 serologic epitope or IEF pattern. B27-HS differs from the six known B27 alleles by five to eight amino acid substitutions, and thus it represents the seventh allele of the HLA-B27 Ag family. This novel B27 allele might have been derived from a gene conversion event. Previously, two amino acid residues at positions 70 and 97 were suggested to be specific for B27 Ag family. B27-HS now reveals that Lys at position 70 is specific for B27 but Asn at position 97 is not. We propose that the region around position 70 might be crucial in determining the B27 serologic epitope and possibly in peptide Ag binding. This study also demonstrates that class I molecules of the same Ag specificity sharing an indistinguishable IEF pattern are not necessarily identical, and indicates that only the definitive determination of primary structure would identify all the class I alleles that are functionally relevant in regard to alloreactivity, T cell restriction, and disease association.

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19

Salvador de Jesús-Bonilla, Vladimir, Mario García-París, Carlos N. Ibarra-Cerdeña, and Alejandro Zaldívar-Riverón. "Geographic patterns of phenotypic diversity in incipient species of North American blister beetles (Coleoptera: Meloidae) are not determined by species niches, but driven by demography along the speciation process." Invertebrate Systematics 32, no. 3 (2018): 672. http://dx.doi.org/10.1071/is17072.

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The Epicauta stigmata complex is a group of blister beetles composed of three parapatric or sympatric species that occur in central Mexico to southern USA: E. stigmata, E. uniforma and E. melanochroa. These species are morphologically very similar, and are mainly distinguished by body colour differences. Here we assessed whether phenotypic divergence in coloration patterns define evolutionary units within the complex. We studied the phylogenetic relationships, demographic history and concordances between morphological and ecological traits in the group. The complex apparently had a demographic history of recent population expansion during the last glaciation period 75000 to 9500 years ago. The three species show no reciprocal monophyly, and thus their allospecificity was not confirmed. The current distribution of haplotypes and the genetic divergences in these taxa can be explained by either recent mitochondrial introgression events caused by hybridisation or by incomplete lineage sorting. Colour pattern differences in the complex are not likely a product of local selection acting over a common genetic background. We suggest that phenotypic divergence in colour patterns during an incipient speciation process might be seen as an enhancing factor of cohesion within each of the three evolutionary units.

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20

Del Porto, P., M. D'Amato, M. T. Fiorillo, L. Tuosto, E. Piccolella, and R. Sorrentino. "Identification of a novel HLA-B27 subtype by restriction analysis of a cytotoxic gamma delta T cell clone." Journal of Immunology 153, no. 7 (October 1, 1994): 3093–100. http://dx.doi.org/10.4049/jimmunol.153.7.3093.

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Abstract Seven HLA-B27 alleles are known, which share the same allospecificity, but differ by one to six amino acid substitutions. Herein, we describe a novel HLA-B27 allele, provisionally named B27-ci, which is expressed by an individual from whom a B27-restricted gamma delta T cell clone has been derived. This clone recognizes B cell lines from the proband and all of the other B27-positive members of the family, but does not lyse B cell lines that express other HLA-B27 alleles. The amino acid sequence deduced from three B27-ci cDNA clones was found to differ from the B*2705 sequence by one amino acid substitution (Asp to His) in position 116 of the alpha 2 domain. This position has been shown to lie in the floor of the F pocket, where it plays a key role in determining the nature of the amino acid side chain that will fit into this pocket. Moreover, the fact that the clone described here possesses a TCR-gamma delta indicates that this subset of cells not only can be HLA-restricted, but also can finely discriminate among classical class I molecules.

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21

Shishida, Masayuki, Hideki Ohdan, Takashi Onoe, Yuka Tanaka, Yuka Igarashi, Masataka Banshodani, and Toshimasa Asahara. "Role of Invariant Natural Killer T Cells in Liver Sinusoidal Endothelial Cell-Induced Immunosuppression Among T Cells with Indirect Allospecificity." Transplantation 85, no. 7 (April 2008): 1060–64. http://dx.doi.org/10.1097/tp.0b013e31816a3372.

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22

Halverson, David C., Gretchen N. Schwartz, Charles Carter, Ronald E. Gress, and Daniel H. Fowler. "In Vitro Generation of Allospecific Human CD8+ T Cells of Tc1 and Tc2 Phenotype." Blood 90, no. 5 (September 1, 1997): 2089–96. http://dx.doi.org/10.1182/blood.v90.5.2089.

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Abstract We have previously shown that allospecific murine CD8+ T cells of the Tc1 and Tc2 phenotype could be generated in vitro, and that such functionally defined T-cell subsets mediated a graft-versus-leukemia (GVL) effect with reduced graft-versus-host disease (GVHD). To evaluate whether analogous Tc1 and Tc2 subsets might be generated in humans, CD8+ T cells were allostimulated in the presence of either interleukin-12 (IL-12) and transforming growth factor-beta (TGF-β) (Tc1 culture) or IL-4 (Tc2 culture). Tc1-type CD8 cells secreted the type I cytokines IL-2 and interferon gamma (IFN-γ), whereas Tc2-type cells primarily secreted the type II cytokines IL-4, IL-5, and IL-10. Both cytokine-secreting populations effectively lysed tumor targets when stimulated with anti–T-cell receptor (TCR) antibody; allospecificity of Tc1- and Tc2-mediated cytolytic function was demonstrated using bone marrow–derived stimulator cells as targets. In addition, both Tc1 and Tc2 subsets were capable of mediating cytolysis through the fas pathway. We therefore conclude that allospecific human CD8+ T cells of Tc1 and Tc2 phenotype can be generated in vitro, and that these T-cell populations may be important for the mediation and regulation of allogeneic transplantation responses.

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23

Jiang, Shuiping, Julia Tsang, David S. Game, Saskia Stevenson, Giovanna Lombardi, and Robert I. Lechler. "Generation and Expansion of Human CD4+CD25+ Regulatory T Cells with Indirect Allospecificity: Potential Reagents to Promote Donor-Specific Transplantation Tolerance." Transplantation 82, no. 12 (December 2006): 1738–43. http://dx.doi.org/10.1097/01.tp.0000244932.29542.9e.

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24

Yuen-Shan Tsang, Julia, Yakup Tanriver, Shuiping Jiang, Eva Leung, Kulachelvy Ratnasothy, Giovanna Lombardi, and Robert Lechler. "Indefinite mouse heart allograft survival in recipient treated with CD4+CD25+ regulatory T cells with indirect allospecificity and short term immunosuppression." Transplant Immunology 21, no. 4 (September 2009): 203–9. http://dx.doi.org/10.1016/j.trim.2009.05.003.

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25

Golshayan, Dela, Shuiping Jiang, Julia Tsang, Marina I. Garin, Christian Mottet, and Robert I. Lechler. "In vitro–expanded donor alloantigen–specific CD4+CD25+ regulatory T cells promote experimental transplantation tolerance." Blood 109, no. 2 (September 26, 2006): 827–35. http://dx.doi.org/10.1182/blood-2006-05-025460.

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Abstract CD4+CD25+ regulatory T (Treg) cells play a critical role in the induction and maintenance of peripheral immune tolerance. In experimental transplantation models in which tolerance was induced, donor-specific Treg cells could be identified that were capable of transferring the tolerant state to naive animals. Furthermore, these cells appeared to have indirect allospecificity for donor antigens. Here we show that in vivo alloresponses can be regulated by donor alloantigen-specific Treg cells selected and expanded in vitro. Using autologous dendritic cells pulsed with an allopeptide from H2-Kb, we generated and expanded T-cell lines from purified Treg cells of CBA mice (H2k). Compared with fresh Treg cells, the cell lines maintained their characteristic phenotype, suppressive function, and homing capacities in vivo. When cotransferred with naive CD4+CD25− effector T cells after thymectomy and T-cell depletion in CBA mice that received CBK (H2k+Kb) skin grafts, the expanded Treg cells preferentially accumulated in the graft-draining lymph nodes and within the graft while preventing CBK but not third-party B10.A (H2k+Dd) skin graft rejection. In wild-type CBA, these donor-specific Treg cells significantly delayed CBK skin graft rejection without any other immunosuppression. Taken together, these data suggest that in vitro–generated tailored Treg cells could be considered a therapeutic tool to promote donor-specific transplant tolerance.

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26

Veerapatharan, Anandharaman, Joseph Pidala, Francisca Beato, and Claudio Anasetti. "Ex vivo expansion of antigen specific Human Regulatory T-cells for the prevention or treatment of Graft-vs.-Host Diseases (145.26)." Journal of Immunology 184, no. 1_Supplement (April 1, 2010): 145.26. http://dx.doi.org/10.4049/jimmunol.184.supp.145.26.

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Abstract Evidence from animal studies has demonstrated that allogeneic regulatory T (Treg) cells expanded ex vivo can be used as effective therapeutic tools in the treatment of allograft rejection and graft-vs.-host disease. However, translating Treg-based therapies from animal models of autoimmunity to human clinical trials requires methods for the isolation and expansion of cells with regulatory function. Currently, no effective approach has been established for selective expansion of human allospecific Treg ex vivo that are anticipated to be more potent and exert more selective immunoregulation than polyclonal Treg. In this study, we show the selective expansion of alloantigen specific human CD4+CD25+CD127- Tregs. CD4+CD25+CD127- Treg were freshly isolated, labeled with CFSE and stimulated by MHC (HLA)-mismatched APC’s, in the presence of IL-2 and IL-15 to amplify the proliferative responses, and sirolimus to suppress other T cells. The expanded Tregs with low CFSE content were sorted by flow cytometry and exhibited suppressive function against CD4 T cell responses. Experiments are underway to selectively expand the antigen specific Tregs with indirect allospecificity. Our data suggest that the antigen specific Tregs can be expanded for the development of Treg cell-based immunotherapy in humans and provides a platform for the selective expansion of Tregs against minor histocompatability antigens to prevent graft-vs.-host disease while sparing graft-vs. -leukemia effects.

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27

Jiang, S., J. Tsang, and R. I. Lechler. "Adoptive Cell Therapy Using In Vitro Generated Human CD4+CD25+ Regulatory T Cells With Indirect Allospecificity to Promote Donor-Specific Transplantation Tolerance." Transplantation Proceedings 38, no. 10 (December 2006): 3199–201. http://dx.doi.org/10.1016/j.transproceed.2006.10.132.

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28

Pistillo, Maria Pia, Nobuyuki Tanigaki, Ramon Chua, Osvaldo Mazzoleni, and Giovan Battista Ferrara. "Human anti-HLA-DQw2 monoclonal antibody secreted by an Epstein-Barr-virus- transformed lymphoblastoid cell line: Assessment of the monoclonality, allospecificity, and target." Human Immunology 24, no. 4 (April 1989): 253–63. http://dx.doi.org/10.1016/0198-8859(89)90019-0.

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29

Claesson, M. H., and R. G. Miller. "Functional heterogeneity in allospecific cytotoxic T lymphocyte clones. II. Development of syngeneic cytotoxicity in the absence of specific antigenic stimulation." Journal of Immunology 134, no. 2 (February 1, 1985): 684–90. http://dx.doi.org/10.4049/jimmunol.134.2.684.

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Abstract Two out of four long-term murine allospecific cytotoxic T lymphocyte (CTL) clones tested could develop high levels of cytotoxicity against syngeneic target cells when cultured under appropriate conditions. All CTL clones maintained strict allospecificity so long as they were cultured with both appropriate allogeneic stimulator cells and growth factor (supernatant from secondary mixed lymphocyte cultures). In two of the clones, syngeneic reactivity rapidly developed when the allogeneic stimulator cells were replaced with syngeneic or third party stimulator cells, and when the supernatant from EL4 thymoma cells stimulated with phorbol ester was used as growth factor. In addition to killing the appropriate allogeneic target, clones with syngeneic reactivity could kill both syngeneic C57BL/6 targets and H-2-congenic BALB.B targets but not third party unrelated targets, suggesting that the self structure recognized was coded for within the major histocompatibility complex. Such clones did not kill the natural killer (NK) target YAC. The results obtained from cold target inhibition and from subcloning at limiting dilution of clones with syngeneic reactivity suggested that both allogeneic and syngeneic reactivity could be expressed by the same individual cell in the CTL clone. The specificity for syngeneic H-2 as opposed to third party H-2 and NK-sensitive target cells, and the observation that both allospecific and syngeneic killing could be partially blocked by anti-Lyt-2 antibody treatment of the CTL, strongly suggested that different recognition structures are involved in CTL-mediated syngeneic cytotoxicity and NK cytotoxicity.

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30

Frasca, L., S. Jurcevic, B. Marinari, E. Piccolella, R. I. Lechler, and G. Lombardi. "Peptide analogues inhibit in vitro the response of T cells with indirect allospecificity and may be used as a strategy to prolong graft survival." Immunology Letters 56 (May 1997): 235. http://dx.doi.org/10.1016/s0165-2478(97)85932-9.

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31

Frasca, L. "Peptide analogues inhibit in vitro the response of T cells with indirect allospecificity and may be used as a strategy to prolong graft survival." Immunology Letters 56, no. 1-3 (May 1997): 235. http://dx.doi.org/10.1016/s0165-2478(97)87770-x.

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32

Vilches, Carlos, Rosario de Pablo, María J. Herrero, María E. Moreno, and Miguel Kreisler. "Molecular cloning and polymerase chain reaction-sequence-specific oligonucleotide detection of the allele encoding the novel allospecificity HLA-Cw6.2 (Cw∗1502) in Spanish gypsies." Human Immunology 37, no. 4 (August 1993): 259–63. http://dx.doi.org/10.1016/0198-8859(93)90509-y.

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33

Jung, Unsu, Jason E. Foley, Andreas A. Erdmann, Michael A. Eckhaus, and Daniel H. Fowler. "CD3/CD28-costimulated T1 and T2 subsets: differential in vivo allosensitization generates distinct GVT and GVHD effects." Blood 102, no. 9 (November 1, 2003): 3439–46. http://dx.doi.org/10.1182/blood-2002-12-3936.

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AbstractAdoptive T-cell therapy using CD3/CD28 co-stimulation likely requires in vivo generation of antigen specificity. Because CD28 promotes TH1/TC1 (T1) or TH2/TC2 (T2) differentiation, costimulation may generate donor T1 or T2 cells capable of differentially mediating allogeneic graft-versus-tumor (GVT) effects and graft-versus-host disease (GVHD). Costimulation under T1 or T2 conditions indeed generated murine TH1/TC1 cells secreting interleukin-2/interferon-γ (IL-2/IFN-γ) or TH2/TC2 cells secreting IL-4/IL-5/IL-10. In vivo, allogeneic T1 cells expanded, maintained T1 secretion, and acquired allospecificity involving IFN-γ and IL-5. In contrast, allogeneic T2 cells expanded less and maintained T2 secretion but did not develop significant allospecificity.Allogeneic, but not syngeneic, T1 cells mediated a GVT effect against host-type breast cancer cells, as median survival time (MST) increased from 25.6 ± 2.6 (tumor controls) to 69.2 ± 5.9 days (P < 1.2 × 10-9). This T1-associated GVT effect operated independently of fasL because T1 cells from gld mice mediated tumor-free survival. In contrast, allogeneic T2 cells mediated a modest, noncurative GVT effect (MST, 29 ± 1.3 days; P < .0019). T1 recipients had moderate GVHD (histologic score, 4 of 12) that contributed to lethality after bone marrow transplantation; in contrast, T2 recipients had minimal GVHD (histologic score, 1 of 12). CD3/CD28 co-stimulation, therefore, generates T1 or T2 populations with differential in vivo capacity for expansion to alloantigen, resulting in differential GVT effects and GVHD.

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&NA;. "ADOPTIVE CELL THERAPY USING IN-VITRO GENERATED HUMAN CD4+CD25HIGH AND CD4+CD25DIM REGULATORY T CELLS WITH INDIRECT ALLOSPECIFICITY TO PROMOTE DONOR-SPECIFIC TRANSPLANTATION TOLERANCE." Transplantation 82, Suppl 2 (July 2006): 312. http://dx.doi.org/10.1097/00007890-200607152-00728.

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Huizinga, TW, RW Kuijpers, M. Kleijer, TW Schulpen, HT Cuypers, D. Roos, and AE von dem Borne. "Maternal genomic neutrophil FcRIII deficiency leading to neonatal isoimmune neutropenia [see comments]." Blood 76, no. 10 (November 15, 1990): 1927–32. http://dx.doi.org/10.1182/blood.v76.10.1927.1927.

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Abstract The healthy mother of a child with transient immune neutropenia was found to be “NA-null.” The mother's neutrophils did not react with anti- NA1 and anti-NA2 antibodies (polyclonal human alloantibodies and mouse monoclonal antibodies). A healthy donor was discovered during routine neutrophil antigen typing whose neutrophils were also “NA-null.” This NA-phenotype was due to the absence of FcRIII (CD16 antigen) on neutrophils as demonstrated with anti-FcRIII monoclonal antibodies. The neutrophils of these two individuals were not able to bind dimeric immunoglobulin G. However, their cells had a normal expression of other phosphatidylinositol (PI)-linked membrane glycoprotein (CD24, CD67, and CLB gran/5 antigens), ruling out the existence of a PI-linkage defect, such as paroxysmal nocturnal hemoglobinuria. The mother (propsitus) had isoantibodies in her blood against neutrophil-FcRIII without allospecificity, apparently produced during pregnancy and responsible for the neutropenia of her child. The expression of FcRIII on natural killer lymphocytes of both individuals was normal. FcRIII is encoded by two separate genes, one (FcRIII-1) for the neutrophil-PI-linked receptor, another (FcRIII-2) for the natural killer cell and macrophage- transmembrane receptor. By messenger RNA and DNA analysis (with an FcRIII-cDNA probe and restriction endonucleases) the neutrophil-FcRIII deficiency appeared to be due to deletion of the FcRIII-1 gene in both individuals, while the FcRIII-2 gene was normally present. The parents of the propositus were found to be heterozygous for this defect. Thus, FcRIII-1 gene deficiency of the mother may be a cause of (iso)immune neutropenia of the newborn. Whether this deficiency may have other clinical consequences has to be studied.

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Huizinga, TW, RW Kuijpers, M. Kleijer, TW Schulpen, HT Cuypers, D. Roos, and AE von dem Borne. "Maternal genomic neutrophil FcRIII deficiency leading to neonatal isoimmune neutropenia [see comments]." Blood 76, no. 10 (November 15, 1990): 1927–32. http://dx.doi.org/10.1182/blood.v76.10.1927.bloodjournal76101927.

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The healthy mother of a child with transient immune neutropenia was found to be “NA-null.” The mother's neutrophils did not react with anti- NA1 and anti-NA2 antibodies (polyclonal human alloantibodies and mouse monoclonal antibodies). A healthy donor was discovered during routine neutrophil antigen typing whose neutrophils were also “NA-null.” This NA-phenotype was due to the absence of FcRIII (CD16 antigen) on neutrophils as demonstrated with anti-FcRIII monoclonal antibodies. The neutrophils of these two individuals were not able to bind dimeric immunoglobulin G. However, their cells had a normal expression of other phosphatidylinositol (PI)-linked membrane glycoprotein (CD24, CD67, and CLB gran/5 antigens), ruling out the existence of a PI-linkage defect, such as paroxysmal nocturnal hemoglobinuria. The mother (propsitus) had isoantibodies in her blood against neutrophil-FcRIII without allospecificity, apparently produced during pregnancy and responsible for the neutropenia of her child. The expression of FcRIII on natural killer lymphocytes of both individuals was normal. FcRIII is encoded by two separate genes, one (FcRIII-1) for the neutrophil-PI-linked receptor, another (FcRIII-2) for the natural killer cell and macrophage- transmembrane receptor. By messenger RNA and DNA analysis (with an FcRIII-cDNA probe and restriction endonucleases) the neutrophil-FcRIII deficiency appeared to be due to deletion of the FcRIII-1 gene in both individuals, while the FcRIII-2 gene was normally present. The parents of the propositus were found to be heterozygous for this defect. Thus, FcRIII-1 gene deficiency of the mother may be a cause of (iso)immune neutropenia of the newborn. Whether this deficiency may have other clinical consequences has to be studied.

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Momburg, F., A. Ziegler, J. Harpprecht, P. Möller, G. Moldenhauer, and G. J. Hämmerling. "Selective loss of HLA-A or HLA-B antigen expression in colon carcinoma." Journal of Immunology 142, no. 1 (January 1, 1989): 352–58. http://dx.doi.org/10.4049/jimmunol.142.1.352.

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Abstract A panel of colorectal carcinomas has been examined immunohistologically with mAb specific for allodeterminants of HLA-A or HLA-B, and with mAb reactive with HLA-A,B,C framework determinants or beta 2-microglobulin. Out of 85 carcinomas, 5 cases were completely negative for all class I Ag in the tumor cell population. Fifteen cases exhibited a differential expression of HLA-A and HLA-B products in all tumor cells or in a subset. Such tumor cells showed strong staining with monomorphic HLA antibodies but failed to stain with certain allospecific mAb. Negativity of tumor cells was scored only when normal stromal cells within the tumor mass were clearly labeled, indicating expression of the particular allodeterminant(s) in the given tissue. Four carcinomas showed a selective loss of HLA-A2 or a non-A2 HLA-A allospecificity in all tumor cells or a major subset, whereas HLA-B Ag were expressed. Seven cases showed a selective loss of the HLA-Bw6 superspecificity in the tumor cell population; HLA-Bw4 and HLA-A Ag were present. Three cases exhibited a combined loss of HLA-A2 and HLA-Bw6 Ag, with non-A2 HLA-A and HLA-Bw4 Ag being expressed. A further case was HLA-Bw6/Bw4 negative in a major tumor cell subset and HLA-A negative in the complementary minor subset. The results show that a considerable proportion of colorectal carcinomas is heterogeneous with regard to HLA-A and HLA-B expression. The reasons for the appearance of tumor subsets with complete loss of class I Ag or selective loss of only HLA-A or HLA-B Ag are not clear, but it is conceivable that some of them arose because they have escaped immunoselection.

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Schuurman, H. J., L. M. Vaessen, J. G. Vos, A. Hertogh, J. G. Geertzema, C. J. Brandt, and J. Rozing. "Implantation of cultured thymic fragments in congenitally athymic nude rats: ignorance of thymic epithelial haplotype in generation of alloreactivity." Journal of Immunology 137, no. 8 (October 15, 1986): 2440–47. http://dx.doi.org/10.4049/jimmunol.137.8.2440.

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Abstract We studied the development of thymus-dependent immunity in congenitally athymic nude rats after implantation of cultured thymic fragments (CTF), particularly the development of in vitro alloreactivity in allogeneic combinations. CTF of DA (RT1a), PVG (RT1c), and RP (RT1p(u,1] origin were implanted in nude rats of WAG (RT1u) origin. In analysis 14 to 18 wk later, all recipients exhibited thymus-dependent immunocompetence assessed by (immuno)-histology of lymphoid organs and responsiveness to in vitro concanavalin A stimulation and in vivo ovalbumin immunization. Control nude animals were unresponsive. Also, in vitro alloreactivity was observed, measured by mixed lymphocyte reaction and cell-mediated lympholysis. The alloresponse to the allogeneic CTF donor haplotype was as to a third party, but that to the recipient was negative. The CTF before implantation were devoid of lymphoid elements and revealed epithelial-like cells as the major component. Cells in CTF showed expression of RT1 class I and class II antigens. CTF at autopsy had the architecture of a normal thymus. In immunohistochemistry using haplotype-specific antibodies, lymphocytes showed RT1u class I expression as in the normal WAG thymus. In the cortex-like area of CTF, stromal cells revealed class I and class II haplotype expression of the donor thymus, but in the medulla-like area, class II haplotype expression was that of the recipient WAG rat. These data indicate that after implantation in nude rats, CTF become populated not only with lymphoid elements, but also with stromal components from the recipient. In induction of thymus-dependent immunity, these acceptor-derived stromal (dendritic) cells may be involved in generation of allospecificity; class I and class II haplotype expression by the donor cortex (epithelial) compartment is ignored in this process.

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Chang, Chien-Chung, Michael Campoli, Nicholas P. Restifo, Xinhui Wang, and Soldano Ferrone. "Immune Selection of Hot-Spot β2-Microglobulin Gene Mutations, HLA-A2 Allospecificity Loss, and Antigen-Processing Machinery Component Down-Regulation in Melanoma Cells Derived from Recurrent Metastases following Immunotherapy." Journal of Immunology 174, no. 3 (January 20, 2005): 1462–71. http://dx.doi.org/10.4049/jimmunol.174.3.1462.

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Labeta, M. O., N. Fernandez, A. Reyes, P. Ferrara, O. Marelli, E. Le Roy, J. Houlihan, and H. Festenstein. "Biochemical analysis of a novel H-2 class I-like glycoprotein expressed in five AKR-(Gross virus) derived spontaneous T cell leukemias." Journal of Immunology 143, no. 4 (August 15, 1989): 1245–53. http://dx.doi.org/10.4049/jimmunol.143.4.1245.

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Abstract The H-2 class I Ag profiles of five spontaneous AKR (H-2K) Gross virus leukemic cell lines were analyzed. A novel H-2 class I, "alloantigen"-like glycoprotein was immunoprecipitated and isolated from all the tumor cell lines using an H-2Dd-specific mAb 35-5-8. The novel Ag was also recognized in vitro by anti-H-2Dd-specific CTL. In addition, DNA from all the thymomas, but not the DNA from normal adult AKR thymic cells showed a transcribed gene detectable with an H-2Dd-specific oligonucleotide probe. The molecular profile of the novel antigen was further studied by two-dimensional gel electrophoresis and analyzed by a computer based image analyzer system and reverse-phase HPLC tryptic peptide mapping. Its molecular pattern was different from the syngeneic H-2Kk, H-2Dk, and the allogeneic H-2Dd gene products. The two-dimensional gel pattern of the novel H-2 class I molecule had a different overall structure reflected in isoelectric point, number, and distribution of polypeptide spots. The tryptic peptide map analysis showed six peaks exclusively identified with the novel Ag. The calculated degree of homology with the corresponding H-2Dd, H-Dk, and H-Kk peptides was 41, 56, and 51%, respectively. In addition, an unusual cell surface distribution of the novel Ag was observed in most of the leukemic lines. The removal of sialic acid residues by neuraminidase treatment facilitated the detection of the allodeterminants by anti-H-2Dd-specific mAb and CTL. Furthermore, we showed that in one AKR tumor line, 424, there is a close association of the novel Ag with the syngeneic class I molecules. Prior preclearance of the syngeneic class I molecules revealed the presence of the H-2Dd-like allospecificity. The genetic and molecular relationship between the expression of this novel class I-like glycoprotein and the recently sequenced Q5 gene is under current investigation.

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Steinle, A., C. Reinhardt, P. Jantzer, and D. J. Schendel. "In vivo expansion of HLA-B35 alloreactive T cells sharing homologous T cell receptors: evidence for maintenance of an oligoclonally dominated allospecificity by persistent stimulation with an autologous MHC/peptide complex." Journal of Experimental Medicine 181, no. 2 (February 1, 1995): 503–13. http://dx.doi.org/10.1084/jem.181.2.503.

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The nature of alloantigens seen by T lymphocytes, in particular the role of peptides in allorecognition, has been studied intensively whereas knowledge about the in vivo emergence, diversity, and the structural basis of specificity of alloreactive T cells is very limited. Here we describe human T cell clones that recognize HLA-B35 alloantigens in a peptide-dependent manner. TCR sequence analysis revealed that several of these allospecific clones utilize homologous TCR: they all express TCRAV2S3J36C1 and TCRBV4S1J2S7C2 chains with highly related CDR3 sequences. Thus peptide-specific alloreactivity is reflected in homologous CDR3 sequences in a manner similar to that described for T cells that recognize nominal peptide/self-MHC complexes. The in vivo frequency of this TCR specificity was studied in unstimulated PBL of the responding cell donor who was not sensitized against HLA-B35. The vast majority (approximately 75%) of the VA2S3J36 junctional regions obtained from two samples of PBL, isolated at a 9-yr interval, encode CDR3 identical or homologous to those of the functionally characterized HLA-B35 allospecific T cells. These data are most easily explained by a model of alloreactivity in which persistent or recurrent exposure to a foreign peptide/self-MHC complex led to the in vivo expansion and long-term maintenance of specific T cells that show fortuitous crossrecognition of an HLA-B35/peptide complex and dominate the alloresponse against HLA-B35.

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Vaage, J. T., C. Naper, G. Løvik, D. Lambracht, A. Rehm, H. J. Hedrich, K. Wonigeit, and B. Rolstad. "Control of rat natural killer cell-mediated allorecognition by a major histocompatibility complex region encoding nonclassical class I antigens." Journal of Experimental Medicine 180, no. 2 (August 1, 1994): 641–51. http://dx.doi.org/10.1084/jem.180.2.641.

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The ability of natural killer (NK) cells to eliminate normal allogeneic hemic cells is well established in several species including mice, rats, and humans. The controlling elements for NK susceptibility in these species map to the major histocompatibility complex (MHC), but in contrast to findings in mice and humans, the mode of inheritance is not always recessive in rats. This finding is not easily explained by the missing self and hemopoietic histocompatibility (Hh) models for NK recognition, and has led to the idea that certain alloantigens may trigger NK cell reactivity. In our in vitro system for assessing rat NK alloreactivity, we have employed target and inhibitor cells from a large panel of MHC congenic, intra-MHC recombinant and MHC mutant rat strains, as well as appropriate F1 hybrids between them, and we show the following: (a) The nonclassical class I (RT1.C) region was most important in determining the susceptibility of target cells to alloreactive NK cells in vitro. Lymphocyte susceptibility to lysis in vivo also mapped to the C region, which supports the concept that the in vivo and in vitro alloreactivity assays reflect the same recognition process. (b) Four different RT1-controlled NK allospecificities (represented by the u, l, a, and n haplotypes) could be discerned when we used polyclonal NK cells from the PVG (RT1c) strain as effector cells. Three of the target specificities recognized were controlled mainly by the RT1.C region. (c) The expression of RT1.C region-controlled parental strain NK allodeterminants could be demonstrated in F1 hybrids heterozygous for the C region alone and were therefore inherited nonrecessively. (d) Loss of an RT1.C region-controlled NK allospecificity could be shown with the MHC mutant LEW.1LM1 rat strain characterized by a genomic deletion of about 100 kb of the C region. Taken together, these observations have demonstrated a major importance of the nonclassical class I region, i.e., RT1.C, in controlling rat NK allorecognition, and have thereby assigned a hitherto undescribed immunological property to this region. Furthermore, some of the present data are consistent with the existence of polymorphic NK-triggering alloantigens that are coded for by the RT1.C region.

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Ciccone, E., D. Pende, O. Viale, A. Than, C. Di Donato, A. M. Orengo, R. Biassoni, S. Verdiani, A. Amoroso, and A. Moretta. "Involvement of HLA class I alleles in natural killer (NK) cell-specific functions: expression of HLA-Cw3 confers selective protection from lysis by alloreactive NK clones displaying a defined specificity (specificity 2)." Journal of Experimental Medicine 176, no. 4 (October 1, 1992): 963–71. http://dx.doi.org/10.1084/jem.176.4.963.

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This study was designed to identify the target molecules of the natural killer (NK) cell-mediated recognition of normal allogeneic target cells. As previously shown, the gene(s) governing the first NK-defined allospecificity (specificity 1) were found to be localized in the major histocompatibility complex region between BF gene and HLA-A. In addition, the analysis of a previously described family revealed that a donor (donor 81) was heterozygous for three distinct NK-defined allospecificities (specificities 1, 2, and 5). HLA variants were derived from the B-Epstein-Barr virus cell line of donor 81 by gamma irradiation followed by negative selection using monoclonal antibodies specific for the appropriate HLA allele. Several variants were derived that lacked one or more class I antigen expressions. These variants were analyzed for the susceptibility to lysis by NK clones recognizing different allospecificities. The loss of HLA-A did not modify the phenotype (i.e., "resistance to lysis"). On the other hand, a variant lacking expression of all class I antigens became susceptible to lysis by all alloreactive clones. Variants characterized by the selective loss of class I antigens coded for by the maternal chromosome became susceptible to lysis by anti-2-specific clones. Conversely, variants selectively lacking class I antigens coded for by paternal chromosome became susceptible to lysis by anti-1 and anti-5 clones (but not by anti-2 clones). Since the Cw3 allele was lost in the variant that acquired susceptibility to lysis by anti-2 clones and, in informative families, it was found to cosegregate with the character "resistance to lysis" by anti-2 clones, we analyzed whether Cw3 could represent the element conferring selective resistance to lysis by anti-2 clones. To this end, murine P815 cells transfected with HLA Cw3 (or with other HLA class I genes) were used as target cells in a cytolytic assay in which effector cells were represented by alloreactive NK clones directed against different specificities. Anti-2-specific clones efficiently lysed untransfected or A2-, A3-, and A24-transfected P815 cells, while they failed to lyse Cw3-transfected cells. NK clones recognizing specificities other than specificity 2 lysed untransfected or Cw3-transfected cells. Thus, the loss of Cw3 resulted in the de novo appearance of susceptibility to lysis, and transfection of the HLA-negative P815 cells with Cw3 resulted in resistance to lysis by anti-2 clones. Therefore, we can infer that Cw3 expression on (both human and murine) target cells confers selective protection from lysis mediated by anti-2 NK clones.

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Veerapathran, Anandharaman, Joseph Pidala, Francisca Beato, Xue-Zhong Yu, and Claudio Anasetti. "High Frequency of Alloantigen-Specific Regulatory T-Cells In Human Blood Allow Rapid Ex Vivo Expansion for Adoptive Therapy." Blood 116, no. 21 (November 19, 2010): 3747. http://dx.doi.org/10.1182/blood.v116.21.3747.3747.

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Abstract Abstract 3747 Evidence from animal studies has demonstrated that allogeneic regulatory T (Treg) cells can be used as effective therapeutic tools in the prevention of allograft rejection and graft-vs-host disease (GVHD). However, translating Treg-based therapies from animal models to human clinical trials requires methods for the isolation and expansion of functional Treg. Loss of function has been a concern for Treg expanded broadly with anti-CD3 and CD28 antibody-coated beads. Based on preclinical data in rodents, allospecific Tregs are anticipated to be more potent and exert more selective immunoregulation than polyclonal Treg in the prevention or treatment of GVHD. Currently, no effective approach has been established for selective expansion of human allospecific Treg ex vivo. In this study, we show the selective direct and indirect recognition of alloantigen by specific human CD4+CD25+CD127− Tregs. CD4+CD25+CD127− Treg were freshly isolated from normal human blood, labeled with CFSE and stimulated by MHC (HLA)-mismatched APC's, in the presence of IL-2 and IL-15 to amplify the proliferative responses, and sirolimus to suppress other T cells. The precursor frequency of the antigen specific Tregs was calculated by Limiting Dilution Analysis and found to be 1/49 -1/138 among all Tregs. The expanded antigen specific Tregs with low CFSE content were in general greater than 90% by days 12–15 in culture. CFSE-low Tregs were sorted by flow cytometry and exhibited complete suppression against CD25-negative CD4 T cell responses up to ratios of 1:100, in contrast CFSE-high Tregs were not suppressive. Ex vivo expanded antigen specific Tregs maintained high Foxp3, retained lymphoid homing receptor CD62L and chemokine receptor CCR7 expression, suggesting that they are functional and able to migrate to lymphoid tissue in vivo. Among the APC's tested, DC was found to be better stimulus with potent suppressive potential when compared to T-cell stimulated PBMC's. Specific indirect allorecognition was elicited when Tregs were stimulated with autologous APC's pulsed with allogeneic cell lysate in the presence of sirolimus, IL-15 and IL-2. Precursor frequency of antigen specific Tregs with indirect allorecognition was 100 fold lower than the precursor frequency of Tregs with direct allospecificity. Highly suppressive antigen specific Tregs show a duplication time of approximately 24 hours in the presence alloantigen, cytokines and sirolimus, and can be expanded in vitro by 400 fold in a 12 day period. This magnitude of expansion predicts the feasibility of conducting translational clinical trials. Our data may provide a platform for the selective expansion of Tregs against minor histocompatibility antigens to prevent GVHD while sparing graft-vs.-leukemia effects. Disclosures: No relevant conflicts of interest to declare.

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Frasca, Loredana, Ayala Tamir, Stipo Jurcevic, Barbara Marinari, Andrea Monizio, Rosa Sorrentino, Maurizio Carbonari, Enza Piccolella, Robert I. Lechler, and Giovanna Lombardi. "PEPTIDE ANALOGUES AS A STRATEGY TO INDUCE TOLERANCE IN T CELLS WITH INDIRECT ALLOSPECIFICITY1." Transplantation 70, no. 4 (August 2000): 631–40. http://dx.doi.org/10.1097/00007890-200008270-00017.

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Mariotti, Jacopo, Jason Foley, Kaitlyn Ryan, Nicole Buxhoeveden, and Daniel Fowler. "Pentostatin Is Advantageous Relative to Fludarabine for in Vivo Murine T Cell Depletion, Suppression of T Cell Cytokine Secretion, and Inhibition of HVGR." Blood 112, no. 11 (November 16, 2008): 3483. http://dx.doi.org/10.1182/blood.v112.11.3483.3483.

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Abstract Although fludarabine and pentostatin are variably utilized for conditioning prior to clinical allogeneic transplantation, limited data exists with respect to their relative efficacy in terms of host immune T cell depletion and T cell suppression. To directly compare these agents in vivo in a murine model, we compared a regimen of fludarabine plus cyclophosphamide (FC) similar to one that we previously developed (Petrus et al, BBMT, 2000) to a new regimen of pentostatin plus cyclophosphamide (PC). Cohorts of mice (n=5–10) received a three-day regimen consisting of P alone (1 mg/kg/d), F alone (100 mg/kg/d), C alone (50 mg/kg/d), or combination PC or FC. Similar to our previous data, administration of P, F, or C alone yielded minimal host T cell depletion (as measured by enumeration of splenic CD4+ and CD8+ T cells) and minimal T cell suppression (as determined by CD3, CD28 co-stimulation of a constant number of remaining splenic T cells and measuring resultant cytokine secretion by multi-analyte assay). The PC and FC regimens were similar in terms of myeloid suppression (p=.2). However, the PC regimen was more potent in terms of depleting host CD4+ T cells (remaining host CD4 number [× 10^6/spleen], 2.1±0.3 [PC] vs. 4.4±0.6 [FC], p<0.01) and CD8+ T cells (remaining host CD8 number, 1.7±0.2 [PC] vs. 2.4±0.5 [FC], p<0.01). Moreover, the PC regimen yielded greater T cell immune suppression than the FC regimen (cytokine values are pg/ml/0.5×10^6 cells/ml; all comparisons p<0.05) with respect to capacity to secrete IFN-γ (13±5 [PC] vs. 48±12 [FC]), IL-2 (59±44 [PC] vs. 258±32 [FC]), IL-4 (34±10 [PC] vs. 104±12 [FC]), and IL-10 (15±3 [PC] vs. 34±5 [FC]). In light of this differential in both immune T cell depletion and suppression of T cell effector function, we hypothesized that T cells from PC-treated recipients would have reduced capacity to mediate a host-versus-graft rejection response (HVGR) relative to FC-treated recipients. To directly test this hypothesis, we utilized a host T cell add-back model of rejection whereby BALB/c hosts were lethally irradiated (1050 cGy; day -2), reconstituted with host-type T cells from PC- or FC-treated recipients (day -1; 0.1 × 10^6 T cells transferred), and finally challenged with fully MHC-disparate transplantation (B6 donor bone marrow cells, 10 × 10^6 cells; day 0). In vivo HVGR was quantified by the following method at day 7 post-BMT: harvest of splenic T cells, stimulation with host- or donor-type dendritic cells, and use of six-color flow cytometry to detect host T cells, CD4 and CD8 subsets, and cytokine secretion by capture method. Consistent with our hypothesis, PC-treated cells acquired greatly reduced alloreactivity in vivo relative to FC-treated cells: the percentage of host CD4+ T cells secreting IFN-γ in an allospecific manner was 2.3±0.8% in recipients of PC-treated T cells and 62.7±13.4% in recipients of FC-treated cells (p<0.001). Similarly, the percentage of host CD8+ T cells secreting IFN-γ in an allospecific manner was 8.6±2.8% in recipients of PC-treated T cells and 92.7±4.1% in recipients of FC-treated T cells (p<0.001). We therefore conclude that at similar levels of myeloid suppression, the PC regimen is superior to the FC regimen in terms of murine T cell depletion, suppression of global T cell cytokine secretion, and inhibition of in vivo capacity to acquire allospecificity in response to fully genetically disparate marrow allografts. These data provide a rationale to develop PC regimens as an alternative to currently utilized FC regimens.

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Frasca, Loredana, Alessandra Amendola, Phil Hornick, Paul Brookes, Gerald Aichinger, Federica Marelli-Berg, Robert Ian Lechler, and Giovanna Lombardi. "ROLE OF DONOR AND RECIPIENT ANTIGEN-PRESENTING CELLS IN PRIMING AND MAINTAINING T CELLS WITH INDIRECT ALLOSPECIFICITY1." Transplantation 66, no. 9 (November 1998): 1238–43. http://dx.doi.org/10.1097/00007890-199811150-00020.

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"Longevity of allospecificity in human T cell clones." Human Immunology 12, no. 2 (February 1985): 129–30. http://dx.doi.org/10.1016/0198-8859(85)90414-8.

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