Статті в журналах: "Allotyping"

1

Guggenheim, Michael. "From Prototyping to Allotyping." Journal of Cultural Economy 7, no. 4 (January 6, 2014): 411–33. http://dx.doi.org/10.1080/17530350.2013.858060.

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2

Ah-See, K. W., T. G. Cooke, and A. Balmain. "Allotyping a human squamous cell carcinoma model." Melanoma Research 3 (September 1993): 50. http://dx.doi.org/10.1097/00008390-199309002-00191.

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3

Field, L. Leigh, and Jean-Michel Dugoujon. "Immunoglobulin allotyping (Gm, Km) of GAW5 families." Genetic Epidemiology 6, no. 1 (1989): 31–33. http://dx.doi.org/10.1002/gepi.1370060108.

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4

ZHANG, W. J., T. J. COBAIN, R. L. DAWKINS, G. GRIMSLEY, and I. R. MACKAY. "Complement Allotyping Explains MHC Associations in Multiple Sclerosis." Annals of the New York Academy of Sciences 540, no. 1 Advances in N (November 1988): 372–73. http://dx.doi.org/10.1111/j.1749-6632.1988.tb27103.x.

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5

Grosse-Wilde, H., and I. Doxiadis. "ALLOTYPING FOR HLA CLASS I USING PLASMA AS ANTIGEN SOURCE." European Journal of Immunogenetics 16, no. 2 (April 1989): 149–55. http://dx.doi.org/10.1111/j.1744-313x.1989.tb00457.x.

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6

Zhang, W. J., P. H. Kay, T. J. Cobain, and R. L. Dawkins. "C4 allotyping on plasma or serum: Application to routine laboratories." Human Immunology 21, no. 3 (January 1988): 165–71. http://dx.doi.org/10.1016/0198-8859(88)90068-7.

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7

Zhang, W., T. J. Cobain, G. Grimsley, I. R. Mackay, and R. L. Dawkins. "Complement allotyping provides explanations for MHC associations found in multiple sclerosis." Journal of Neuroimmunology 16, no. 1 (September 1987): 192–93. http://dx.doi.org/10.1016/0165-5728(87)90430-9.

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8

Kumar, N., G. Kaur, N. Tandon, and N. K. Mehra. "Allotyping human complement factor B in Asian Indian type 1 diabetic patients." Tissue Antigens 72, no. 6 (December 2008): 517–24. http://dx.doi.org/10.1111/j.1399-0039.2008.01137.x.

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9

Kay, P. H., J. McCluskey, F. T. Christiansen, D. Feeney, V. J. McCann, P. J. Zilko, R. L. Dawkins, and G. J. O'Neill. "Complement allotyping reveals new genetic markers in rheumatoid arthritis and diabetes mellitus." Tissue Antigens 21, no. 2 (December 11, 2008): 159–60. http://dx.doi.org/10.1111/j.1399-0039.1983.tb00383.x.

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10

Leppers-van de Straat, F. G. J., W.-L. van der Pol, M. D. Jansen, N. Sugita, H. Yoshie, T. Kobayashi та J. G. J. van de Winkel. "A novel PCR-based method for direct Fcγ receptor IIIa (CD16) allotyping". Journal of Immunological Methods 242, № 1-2 (серпень 2000): 127–32. http://dx.doi.org/10.1016/s0022-1759(00)00240-4.

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11

Christiansen, F. T., R. E. Bontrop, M. Giphart, P. U. Cameron, W. J. Zhang, D. Townend, M. Jonker, and R. L. Dawkins. "Major histocompatibility complex ancestral haplotypes in the chimpanzee: Identification using C4 allotyping." Human Immunology 31, no. 1 (May 1991): 34–39. http://dx.doi.org/10.1016/0198-8859(91)90046-c.

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12

Doxiadis, Gabriele, and Hans Grosse-Wilde. "C4 Allotyping by Prolonged Gel Electrophoresis and Immunoblotting Using Monoclonal and Polyclonal Antibodies." Complement and Inflammation 7, no. 4-6 (1990): 269–76. http://dx.doi.org/10.1159/000463160.

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13

Cohen, Brian B., Valerie A. Anderson, and Karen Gillespie. "Artefactual Allotyping Related to DNA Source, Concentration and the Number of PCR Cycles." Disease Markers 14, no. 3 (1998): 165–67. http://dx.doi.org/10.1155/1998/629481.

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14

Uko, G., F. T. Christiansen, and R. L. Dawkins. "Serum C4 concentration in the monitoring of systemic lupus erythematosus: requirement for C4 allotyping." Rheumatology International 6, no. 3 (July 1986): 111–14. http://dx.doi.org/10.1007/bf00270346.

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15

Kölble, Konrad, Vesna Rukavina, and Joachim R. Kalden. "High resolution electrophoresis for the allotyping of human C4 Proposal of a relational nomenclature." Journal of Immunological Methods 96, no. 1 (January 1987): 69–76. http://dx.doi.org/10.1016/0022-1759(87)90369-3.

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16

Bayer, P. A., and M. Tsipis. "Extended liquid nitrogen storage of erythrocytes coated with purified monoclonal proteins for Gm allotyping." Journal of Immunological Methods 113, no. 2 (October 1988): 289–90. http://dx.doi.org/10.1016/0022-1759(88)90345-6.

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17

Balbín, Milagros, Anders Grubb, Gerda G. de Lange, and Rune Grubb. "DNA sequences specific for Caucasian G3m(b) and (g) allotypes: allotyping at the genomic level." Immunogenetics 39, no. 3 (January 1994): 187–93. http://dx.doi.org/10.1007/bf00241259.

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18

Swanson, Jane L., Robert M. Sastamoinen, Theresa A. Steeper, and Elizabeth S. Sebring. "Gm Allotyping to Determine the Origin of Red Cell Antibodies in Recipients of Solid Organ Transplants." Vox Sanguinis 52, no. 1-2 (1987): 75–78. http://dx.doi.org/10.1159/000461614.

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19

Swanson, Jane L., Robert M. Sastamoinen, Theresa A. Steeper, and Elizabeth S. Sebring. "Gm Allotyping to Determine the Origin of Red Cell Antibodies in Recipients of Solid Organ Transplants." Vox Sanguinis 52, no. 1-2 (March 1987): 75–78. http://dx.doi.org/10.1111/j.1423-0410.1987.tb02994.x.

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20

Egan, L. J., A. Orren, J. Doherty, R. Würzner, and C. F. McCarthy. "Hereditary deficiency of the seventh component of complement and recurrent meningococcal infection: investigations of an Irish family using a novel haemolytic screening assay for complement activity and C7 M/N allotyping." Epidemiology and Infection 113, no. 2 (October 1994): 275–81. http://dx.doi.org/10.1017/s0950268800051700.

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SUMMARYTerminal complement component deficiency predisposes to meningococcal infection and is inherited in an autosomal co-dominant manner. An Irish family is described, in which 2 of 3 brothers had recurrent meningococcal infection. A novel screening assay was used to investigate for terminal complement deficiency and the 2 affected brothers were found to be completely deficient in the seventh component of complement (C7). Enzyme-linked immunosorbent assay for C7 revealed lower than normal levels in the remaining brother and parents. C7 M/N protein polymorphism allotyping, used to investigate the segregation of the C7 deficiency genes, showed that the apparently complement sufficient brother was heterozygous C7 deficient and a carrier of one of the deficiency genes. Complement screening should be carried out in any individual suffering recurrent meningococcal infection or infection with an uncommon meningococcal serogroup. Identification of complement deficient patients allows the implementation of strategies to prevent recurrent infection.

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21

Swanson, Jane, Elizabeth Sebring, Robert Sastamoinen, and Michael Chopek. "Gm Allotyping to Determine the Origin of the Anti-D Causing Hemolytic Anemia in a Kidney Transplant Recipient." Vox Sanguinis 52, no. 3 (1987): 228–30. http://dx.doi.org/10.1159/000461654.

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22

Swanson, Jane, Elizabeth Sebring, Robert Sastamoinen, and Michael Chopek. "Gm Allotyping to Determine the Origin of the Anti-D Causing Hemolytic Anemia in a Kidney Transplant Recipient." Vox Sanguinis 52, no. 3 (April 1987): 228–30. http://dx.doi.org/10.1111/j.1423-0410.1987.tb03033.x.

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23

KORVER, KEES, GERDA G. DE LANGE, RENÉE LANGLOIS VAN DEN BERGH, PETER TH A. SCHELLEKENS, ERNA VAN LOGHEM, FRED VAN LEEUWEN, and JAAK M. VOSSEN. "LYMPHOID CHIMERISM AFTER ALLOGENEIC BONE MARROW TRANSPLANTATION Y-CHROMATIN STAINING OF PERIPHERAL T AND B LYMPHOCYTES AND ALLOTYPING OF SERUM IMMUNOGLOBULINS." Transplantation 44, no. 5 (November 1987): 643–49. http://dx.doi.org/10.1097/00007890-198711000-00010.

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24

Dechant, Michael, Thomas Poellot, Ulrich Kunzendorf та Thomas Valerius. "Heterogeneous Expression of the 158V and 158F Alleles in FcγRIIIA Heterozygous Donors." Blood 104, № 11 (16 листопада 2004): 1362. http://dx.doi.org/10.1182/blood.v104.11.1362.1362.

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Abstract Recent clinical studies demonstrated that a bi-allelic polymorphism in the human FCGRIIIA gene critically determines the clinical outcome of rituximab therapy in certain hematologic malignancies and in autoimmune diseases. Thus, patients homozygous for the 158V allele of the FcγRIIIa receptor demonstrated significantly better response rates to rituximab therapy compared to homozygous 158F donors. However, confliciting data were reported for heterozygous patients - which account for approximately 45 % of the investigated population. Furthermore, most of the in vitro reports about functional effects of this polymorphism did not address the function of 158V/F heterozygotes. In all these studies, genomic DNA was used for allotyping of the FCGRIIIA 158V/F polymorphism. Thus, these studies were not set up to investigate potential allele- specific differences at mRNA or protein levels, which were demonstrated for several other NK cell- related genes. Therefore, we were interested to analyze receptor expression and function in 158V/F heterozygous donors in more detail. First, we established FCGRIIIA allotyping at the mRNA level. Thus, isolated mRNA was reversely transcribed, PCR amplified and sequenced using BigDye terminator mix. Results from homozygous donors were consistent and homogeneous, whereas sequencing profiles from heterozygotes appeared heterogeneous. Some 158V/F heterozygotes demonstrated similar expression of both alleles, whereas sequencing profiles in others were almost similar to either homozygous 158V/V or homozygous 158F/F donors. Next, we analyzed the quantitative expression of the corresponding proteins by immunofluorescence experiments with antibodies 3G8 and MEM-154. While 3G8 binds similarly to both allelic forms of FcγRIIIa, MEM-154 preferentially recognizes the 158V allele, as confirmed by immunofluorescence studies with FcγRIIIa 158F or 158V transfected cell lines. These experiments again demonstrated that FcγRIIIA 158V/F heterozygous donors are a heterogeneous group - with 158V protein levels ranging from similar to 158F/F homozygotes to similar to 158V/V homozygous donors. Furthermore, we investigated whether 158V expression levels have functional implications in classical 51Cr- release assays against ARH-77 B cells. We used isolated NK cells as effector cells, and rituximab as sensitizing antibody. Effector cells were isolated from matched sets of FCγRIIIA allotyped donors to directly compare 158V/V or 158F/F homozygotes with 158V/F heterozygotes. As described by others, we observed statistically significant differences between 158V/V and 158F/F homozygous donors at suboptimal antibody concentrations. Interestingly, NK cells from 158F/V heterozygous donors, which appeared similar by sequencing profiles and by immunofluorescence studies to effector cells from 158V/V homozygotes, also demonstrated killing levels similar to those from 158V/V homozygous donors. In conclusion, our data demonstrate that donors heterozygous for FcγRIIIA at position 158 are a heterogeneous population - potentially explaining controversial data published about 158F/V heterozygotes in clinical studies. In order to further assess the biological impact of our results, clinical trials may address whether FcγRIIIA 158V expression levels will correlate with clinical responses to rituximab therapy. These studies could help to predict which patients may optimally benefit from rituximab therapy.

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25

Safa, Majid, Mehdi Forouzande, Aliakbar Pourfathol, Pooria Gill, Mohammad Javad Rasaee, Fatemeh Yari, Atefeh Shahbazi, Mohammad Soleiman Soltanpour, and Neema Mayor. "High Resolution Allotyping of Four Alleles of HLA-DRB1*01 Group in Iranians Using Reverse-SSOPH Assay in Comparison with DNA Sequencing and PCR-SSP." Journal of Biological Sciences 8, no. 2 (February 1, 2008): 392–97. http://dx.doi.org/10.3923/jbs.2008.392.397.

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26

Giglio, Fabio, Ted A. Gooley, Jeffrey M. Venstrom, Meighan M. Gallagher, LiHua Hou, Carolyn K. Hurley, Tatiana Lebedeva, et al. "Donor KIR3DL1 and HLA-B Allotypes Control Leukemia Relapse After Allogeneic Hematopoietic Stem Cell Transplantation." Blood 120, no. 21 (November 16, 2012): 349. http://dx.doi.org/10.1182/blood.v120.21.349.349.

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Abstract Abstract 349 Natural killer (NK) cells are vital in the control of viral infection and malignancy, in particular AML. Affinity strength between NK receptors and their HLA ligands control both NK effector function and degree of NK inhibition. Differences in binding affinity between allotypes of the NK receptor KIR3DL1 and allotypes of its ligand HLA-Bw4 depend on the expression levels of the receptor and the amino acid residue at position 80 in the ligand. Because receptor-ligand affinities are associated with differences in HIV control, we hypothesized that different affinities between donor KIR3DL1 and donor-recipient HLA-Bw4 allotypes would impact the risk for AML relapse following allogeneic hematopoietic stem cell transplantation (HCT). Methods: We evaluated 299 AML patients who underwent allogeneic HCT from an unrelated donor between 1995 and 2002. Clinical data, HLA allotyping, and donor DNA were provided by the CIBMTR. KIR3DL1 allotyping was executed using PCR- and sequence-based methods. Donors were segregated into those with high-, low- and null expressing KIR3DL1 allele groups [3DL1-H (n=130), 3DL1-L (n=69), 3DL1-N (n=82)] and HLA-B allele groups (Bw6/Bw6, Bw4-I80, Bw4-T80). 3DL1-N genotypes are predictive of poor surface expression and were analyzed separately. Patients and donors were matched at 9 or 10 HLA loci in all cases, with only 3 donor-patient pairs mismatched for HLA-Bw4 ligands. Affinity cohorts were compared using Cox regression for the time-to-event outcomes of relapse and overall mortality (OM). Kaplan-Meier estimates of overall survival and cumulative incidence estimates of relapse were obtained. Results: Recipients of 3DL1-H and 3DL1-L donors were analyzed for high and low-affinity associations with post-HCT AML relapse. Among patients with a 3DL1-H donor, those transplanted from donors with the low-affinity KIR/HLA allotype combination 3DL1-H/Bw4-T80 had lower risk of relapse when compared to those with the high-affinity 3DL1-H/Bw4-I80 combination (HR 0.22; p=.003, Table) and even moreso when compared to the extra-high affinity combinations of 3DL1-H with Bw4-I80-B*2702 or B*57 (HR 0.10; p<.001). Among patients with 3DL1-L donors, those with the low-affinity KIR-HLA combination 3DL1-L/Bw4-I80 were associated with lower relapse in patients when compared to those with the high-affinity 3DL1-L/Bw4-T80 combination (HR 0.21; P=.009). Among the combined patient groups, low-affinity combinations were strongly associated with lower relapse (HR 0.24; P<.001; FigA) and lower mortality (HR 0.62; P=.03; FigB) in patients compared to the high-affinity combinations. Lack of HLA-Bw4 ligand (HLA-Bw6/Bw6) provided intermediate protection from AML relapse compared to patients in the high-affinity group (HR 0.39; P= .002; Fig 1A). Donor 3DL1-N genotypes, predictive of poor receptor expression on the NK cell surface, were not associated with HCT outcome. Conclusions: Protection from relapse of AML after unrelated HCT is associated with the affinity between donor KIR3DL1 and HLA-Bw4, ranging from the highly protective low-affinity donor KIR3DL1/HLA-Bw4 allotype combinations to the susceptible and “super-susceptible” effects of high- and extra-high affinity KIR/HLA combinations. These data support the consideration of KIR and HLA allotype combinations in stem cell donor selection algorithms to minimize the risk of AML relapse following HCT. Because >95% of donors are positive for KIR3DL1 and 69% of patients are positive for HLA-Bw4, incorporation of KIR3DL1/HLA-Bw4 allotypes in donor selection algorithms is a highly relevant and feasible goal. Disclosures: No relevant conflicts of interest to declare.

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27

Pamphilon, DH, AA Alnaqdy, V. Godwin, AW Preece, and TB Wallington. "Studies of allogeneic bone marrow and spleen cell transplantation in a murine model using ultraviolet-B light." Blood 77, no. 9 (May 1, 1991): 2072–78. http://dx.doi.org/10.1182/blood.v77.9.2072.2072.

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Abstract Ultraviolet irradiation inhibits alloreactive and mitogen-induced responses and might reduce both graft-versus-host and host-versus-graft reactions after bone marrow transplantation (BMT). We have studied proliferative responses to mitogens and reactivity in mixed lymphocyte culture after irradiation with ultraviolet (UV)-B light using splenocytes from Balb/c (H-2d) and CBA (H-2k) mice. Response to mitogens and in MLC was strongly inhibited by 20 J/m2 and abolished at 50 J/m2. Clonogenic cell recovery (CFU-GM; CFU-S) after UV-B irradiation was also reduced. When bone marrow and spleen cells were transplanted from parent (Balb/c) animals into F1 hybrid (Balb/c X CBA) recipients, all animals died with features indicative of graft-versus- host disease (GVHD) in 34 days. If the grafts were first irradiated with 100 J/m2 of UV-B at a mean wavelength of 310 nm, then 76% survived to day 80 when they were killed and shown to have normal marrow cellularity. The remainder died in marrow aplasia or of GVHD. H-2 typing in a group of surviving recipients showed either donor hematopoiesis only (8 of 15), mixed allogeneic chimerism (5 of 15), or recipient type hematopoiesis (2 of 15). Higher doses (200 to 300 J/m2) were detrimental to survival with 88% of recipients dying in marrow aplasia. Syngeneic BMT in Balb/c mice showed slower hematopoietic reconstitution when the grafts were first irradiated with 100 J/m2. After BMT from Balb/c to CBA mice all recipients of unirradiated grafts died within 54 days. By contrast, after graft irradiation with 100 J/m2 survival of recipient animals to day 80 was 59%. If these grafts were treated with 50 J/m2 survival was only 26% with an increase in deaths due to GVHD. Hematopoiesis at day 80 in a group of survivors studied by Ig heavy chain allotyping indicated donor type hematopoiesis in 6 of 10 (50 J/m2) and 2 of 9 (100 J/m2). These data indicate that UV-B irradiation inhibits lymphocyte reactivity and can prevent GVHD. However, there is clear in vitro and in vivo evidence of stem cell damage, such that autologous marrow recovery was demonstrated in a proportion of recipients. In parent----F1 UV-irradiated transplants, sustained hematopoietic recovery was effected in the majority by donor stem cells.

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28

Pamphilon, DH, AA Alnaqdy, V. Godwin, AW Preece, and TB Wallington. "Studies of allogeneic bone marrow and spleen cell transplantation in a murine model using ultraviolet-B light." Blood 77, no. 9 (May 1, 1991): 2072–78. http://dx.doi.org/10.1182/blood.v77.9.2072.bloodjournal7792072.

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Ultraviolet irradiation inhibits alloreactive and mitogen-induced responses and might reduce both graft-versus-host and host-versus-graft reactions after bone marrow transplantation (BMT). We have studied proliferative responses to mitogens and reactivity in mixed lymphocyte culture after irradiation with ultraviolet (UV)-B light using splenocytes from Balb/c (H-2d) and CBA (H-2k) mice. Response to mitogens and in MLC was strongly inhibited by 20 J/m2 and abolished at 50 J/m2. Clonogenic cell recovery (CFU-GM; CFU-S) after UV-B irradiation was also reduced. When bone marrow and spleen cells were transplanted from parent (Balb/c) animals into F1 hybrid (Balb/c X CBA) recipients, all animals died with features indicative of graft-versus- host disease (GVHD) in 34 days. If the grafts were first irradiated with 100 J/m2 of UV-B at a mean wavelength of 310 nm, then 76% survived to day 80 when they were killed and shown to have normal marrow cellularity. The remainder died in marrow aplasia or of GVHD. H-2 typing in a group of surviving recipients showed either donor hematopoiesis only (8 of 15), mixed allogeneic chimerism (5 of 15), or recipient type hematopoiesis (2 of 15). Higher doses (200 to 300 J/m2) were detrimental to survival with 88% of recipients dying in marrow aplasia. Syngeneic BMT in Balb/c mice showed slower hematopoietic reconstitution when the grafts were first irradiated with 100 J/m2. After BMT from Balb/c to CBA mice all recipients of unirradiated grafts died within 54 days. By contrast, after graft irradiation with 100 J/m2 survival of recipient animals to day 80 was 59%. If these grafts were treated with 50 J/m2 survival was only 26% with an increase in deaths due to GVHD. Hematopoiesis at day 80 in a group of survivors studied by Ig heavy chain allotyping indicated donor type hematopoiesis in 6 of 10 (50 J/m2) and 2 of 9 (100 J/m2). These data indicate that UV-B irradiation inhibits lymphocyte reactivity and can prevent GVHD. However, there is clear in vitro and in vivo evidence of stem cell damage, such that autologous marrow recovery was demonstrated in a proportion of recipients. In parent----F1 UV-irradiated transplants, sustained hematopoietic recovery was effected in the majority by donor stem cells.

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29

Cen, Xue Qi, Xiao Dong Wu, Shu Wei, Xi Shun Zhang, Jia Ming Zhang, Jing Fei Tang, and Shu Dong Li. "Research for Calculation Model of Allotypic Pumping Unit Load." Applied Mechanics and Materials 527 (February 2014): 121–29. http://dx.doi.org/10.4028/www.scientific.net/amm.527.121.

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A research has been developed for calculation models of allotypic pumping units load against a series of problems, which are ubiquitous in the oil field, such as unreasonable selection of the pumping unit type, low capacity factor of the pumping unit load, lacking of computing method of allotypic pumping unit load, etc. In the research, a calcaulation model of polished rod motion parameters has been firstly established according to the architectural feature of offset pumping units, dual horsehead pump units and tower pumping units. Then the load calculation model of allotypic pumping units were built based on the superposition method of each rod string stress. And after validating the load models in the oil field, the results have been indicated that the models have been in good agreement with the polished rod load. Therefore, the load calculation model of allotypic pumping units in this paper will be of some guidance significance to the selection of the pumping unit type and the stress check of the rod string in the oil field.

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30

Shulman, Stanford T., Marian Melish, Osmu Inoue, Hirohisa Kato, and Shobun Tomita. "Immunoglobulin allotypic markers in Kawasaki disease." Journal of Pediatrics 122, no. 1 (January 1993): 84–86. http://dx.doi.org/10.1016/s0022-3476(05)83493-6.

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31

Grubb, Rune. "Stimuli for Anti-Ig-allotypic antibodies." Clinical Immunology Newsletter 6, no. 11 (November 1985): 161–63. http://dx.doi.org/10.1016/s0197-1859(85)80062-5.

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32

Schreier, P. H., S. Quester та A. Bothwell. "Allotypic differences in murine μ genes". Nucleic Acids Research 14, № 5 (1986): 2381–89. http://dx.doi.org/10.1093/nar/14.5.2381.

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33

Kickler, TS, PM Ness, HG Braine, L. Richardson, and M. Farkosh. "The expression of IgG allotypes on platelets and immunization to IgG allotypes in multitransfused thrombocytopenic patients." Blood 76, no. 4 (August 15, 1990): 849–52. http://dx.doi.org/10.1182/blood.v76.4.849.849.

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Abstract We investigated whether the platelet-membrane surface carries IgG allotypic antigens and whether these determinants may be important in platelet transfusion therapy. Using a hemagglutination inhibition assay, we showed that the G1m IgG allotypes (a, x, f) and K1m and K3m light-chain allotypes are expressed on the surface of platelets, whereas G3m allotype antigenic determinants were not detectable. In 146 multitransfused thrombocytopenic patients, 35 (24%) patients were found to have antiallotypic antibodies. To study the effect of antiallotypic antibodies on platelet transfusion outcome, patients received platelet transfusions from donors, either positive or negative for the IgG allotype to which patients were immunized. Of the 19 antigen-positive and 19 antigen-negative platelet transfusions given, respectively, the mean platelet count increments at 1 hour were 8,402 +/- 6,402 +/- 6,721 (1 SD) and 9,799 +/- 5,559 (1 SD) P less than .2. Transfusion reactions were not more common when antigen-positive platelet transfusions were given. Despite the presence of IgG allotypic determinants on platelets, allotypic antibodies do not decrease platelet transfusion recovery. Furthermore, passive administration of plasma containing IgG allotypes to patients with antiallotypic antibodies does not lead to innocent bystander-mediated platelet destruction.

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34

Kickler, TS, PM Ness, HG Braine, L. Richardson, and M. Farkosh. "The expression of IgG allotypes on platelets and immunization to IgG allotypes in multitransfused thrombocytopenic patients." Blood 76, no. 4 (August 15, 1990): 849–52. http://dx.doi.org/10.1182/blood.v76.4.849.bloodjournal764849.

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Анотація:

We investigated whether the platelet-membrane surface carries IgG allotypic antigens and whether these determinants may be important in platelet transfusion therapy. Using a hemagglutination inhibition assay, we showed that the G1m IgG allotypes (a, x, f) and K1m and K3m light-chain allotypes are expressed on the surface of platelets, whereas G3m allotype antigenic determinants were not detectable. In 146 multitransfused thrombocytopenic patients, 35 (24%) patients were found to have antiallotypic antibodies. To study the effect of antiallotypic antibodies on platelet transfusion outcome, patients received platelet transfusions from donors, either positive or negative for the IgG allotype to which patients were immunized. Of the 19 antigen-positive and 19 antigen-negative platelet transfusions given, respectively, the mean platelet count increments at 1 hour were 8,402 +/- 6,402 +/- 6,721 (1 SD) and 9,799 +/- 5,559 (1 SD) P less than .2. Transfusion reactions were not more common when antigen-positive platelet transfusions were given. Despite the presence of IgG allotypic determinants on platelets, allotypic antibodies do not decrease platelet transfusion recovery. Furthermore, passive administration of plasma containing IgG allotypes to patients with antiallotypic antibodies does not lead to innocent bystander-mediated platelet destruction.

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35

Full, Christine, J. N. Meyer, H. Brandt, and P. Glodek. "Die Allotypen der Lipoproteine und Globuline beim Schwein." Journal of Animal Breeding and Genetics 107, no. 1-6 (January 12, 1990): 221–28. http://dx.doi.org/10.1111/j.1439-0388.1990.tb00029.x.

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36

Full, Christine, J. N. Meyer, and P. Glodek. "Die Allotypen der Lipoproteine und Globuline beim Schwein." Journal of Animal Breeding and Genetics 107, no. 1-6 (January 12, 1990): 261–68. http://dx.doi.org/10.1111/j.1439-0388.1990.tb00035.x.

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37

Mirzaei, Hamid, and Fred Regnier. "Creation of Allotypic Active Sites during Oxidative Stress." Journal of Proteome Research 5, no. 9 (September 2006): 2159–68. http://dx.doi.org/10.1021/pr060021d.

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38

McCartney-Francis, Nancy, Eduardo A. Padlan, Gerson H. Cohen, and Rose G. Mage. "Localization of rabbit kappa light chain allotypic determinants." Molecular Immunology 23, no. 5 (May 1986): 475–88. http://dx.doi.org/10.1016/0161-5890(86)90111-2.

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39

Seppälä, I. J., H. Sarvas, and O. Mäkelä. "Low concentrations of Gm allotypic subsets G3 mg and G1 mf in homozygotes and heterozygotes." Journal of Immunology 151, no. 5 (September 1, 1993): 2529–37. http://dx.doi.org/10.4049/jimmunol.151.5.2529.

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Abstract Serum concentrations of IgG3, IgG1, and of the Gm allotypic subsets of these two isotypes were measured in adult homozygotes and heterozygotes. Alleles G3 mb and G3 mst of the IgG3 locus, and alleles G1 ma and G1 max of the IgG1 locus were found to associate with a high concentration of the allotypic product. Alleles G3 mg (IgG3) and G1 mf (IgG1) were associated with a low concentration of the product. This was true regardless of the haplotype; for example, allele G3 mb was associated with a high concentration of the product in all haplotypes f;n+;b f;n-;b and fa;n+;b. One dose of allele G3 mg was associated with a characteristic mean concentration of the product (g-type IgG3). This rule was valid regardless of the other allele of the subject, thus, heterozygotes and G3 mg/g homozygotes had mean concentrations of 0.10 and 0.20 g/liter, respectively, of g-type IgG3. Products of the IgG1 alleles were also simply additive: one dose of allele G1 ma(x) or G1 mf was associated with mean concentrations of 3.63 and 2.84 g/liter, respectively, and two doses with twice these amounts. Only allele G3 mb did not completely follow this rule. We also studied the serum concentrations and the allotype distribution of 41 IgG1 and 31 IgG3 myeloma proteins. The results suggested that the allotype-associated differences in serum concentrations are caused by different numbers of B cells producing allotypic subsets of IgG1 or IgG3, not by different rates of synthesis per B cell.

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40

MINAMI, S., R. UEDA, T. SHIRAKI, M. TANIMOTO, R. NAMIKAWA, M. SETO, K. NISHIDA, I. TSUGE, K. OTA, and T. TAKAHASHI. "Two monoclonal antibodies detecting allotypic determinants of HLA-A." Tissue Antigens 22, no. 4 (December 11, 2008): 239–45. http://dx.doi.org/10.1111/j.1399-0039.1983.tb01199.x.

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41

Ito, Shigenori, Koichi Suzuki, Tokiko Miyazaki, and Hideo Matsumoto. "A key amino acid determining G3m(b) allotypic markers." Japanese journal of human genetics 36, no. 2 (June 1991): 179–87. http://dx.doi.org/10.1007/bf01876582.

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42

Butler, J. E., H. Heyermann, M. Borca, M. Bielecka, and L. V. Frenyo. "The isotypic, allotypic and idiotypic heterogeneity of bovine IgG2." Veterinary Immunology and Immunopathology 17, no. 1-4 (December 1987): 1–16. http://dx.doi.org/10.1016/0165-2427(87)90122-x.

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43

Benaroch, P., and G. Bordenave. "T-cell-induced chronic immunoglobulin allotypic suppression in mouse." Research in Immunology 140, no. 3 (January 1989): 307–13. http://dx.doi.org/10.1016/0923-2494(89)90068-0.

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44

Benaroch, P., and G. Bordenave. "T cell-induced Ig allotypic suppression in mice. II. Both CD4+ CD8- and CD4- CD8+ T cell subsets from sensitized Igha mice are required to induce suppression of Igh-1b allotype expression." Journal of Immunology 142, no. 1 (January 1, 1989): 1–7. http://dx.doi.org/10.4049/jimmunol.142.1.1.

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Abstract We established the phenotype of T splenocytes (Ts) from Igha/a BALB/c mice sensitized against B splenocytes from the Ighb/b CB20 congenic mice that induce Igh-1b (IgG2a of the Ighb haplotype) suppression. This was achieved by studying the action of anti-T cell subset mAb on the capacity of Ts to induce this chronic allotypic suppression in Igha/b (BALB/c x CB20)F1 mice. The Ts were treated with cytotoxic anti-mouse CD4 or anti-mouse CD8 rat mAb in vitro before their injection into the Igha/b newborns or in vivo after their injection into the Igha/b newborns. Exposure to either anti-CD8 or anti-CD4 mAb in vitro or in vivo leads to loss of the capacity of Ts to induce Igh-1b allotypic suppression. Mixing CD4+-cell-depleted Ts and CD8+-cell-depleted Ts preparations restored the capacity of the cells to induce Igh-1b suppression. Thus, both CD4+ CD8- Ts and CD4- CD8+ Ts are required for the induction of this allotypic suppression. Bone marrow cells and B splenocytes from Igh-1b-suppressed adult Igha/b mice were shown to be able to durably express Igh-1b when transferred into irradiated Igha/a BALB/c hosts whereas whole spleen cells from such donors failed to do it. Abrogation of Igh-1b suppression by in vivo anti-CD8 mAb treatment was achieved in adult Igha/b heterozygotes but with a lower efficiency than in adult Ighb/b homozygotes, all being chronically Igh-1b suppressed. The CD4- CD8+ cell population essential for maintaining this suppression is resistant to in vivo 600 rad irradiation and seems to be slightly inhibited by in vivo administration of free Igh-1b.

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45

Zitouni, M., P. Martel, M. Ben Ayed, G. Raux, D. Gilbert, P. Joly, I. Mokhtar, et al. "Pemphigus is not associated with allotypic markers of immunoglobulin kappa." Genes & Immunity 3, no. 1 (February 2002): 50–52. http://dx.doi.org/10.1038/sj.gene.6363817.

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46

Shaffer, Brian C., Glenn Heller, Jean-Benoit Le Luduec, Jack Vahradian, Miguel Perales, Sergio A. Giralt, Roni Tamari, et al. "Selection of Unrelated Allogeneic Hematopoietic Cell Donors Based on KIR3DL1 Allotypes Is Feasible and Results in Improved Disease-Free Survival in Transplant Recipients with MDS and AML." Blood 128, no. 22 (December 2, 2016): 990. http://dx.doi.org/10.1182/blood.v128.22.990.990.

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Abstract Donor natural killer (NK) cells impart a potent anti-leukemia effect after allogeneic hematopoietic cell transplantation (allo HCT). The killer Ig-like receptors (KIR) play a central role in modulating NK effector function. Chief among them, the inhibitory KIR3DL1 exhibits a high degree of allelic polymorphism. We previously demonstrated that highly expressed KIR3DL1 alleles (KIR3DL1 allele groups *001 and *002) bind preferentially to HLA-Bw4 with I80 to confer a high degree of inhibitory signaling. Similarly, poorly expressed KIR3DL1 alleles (KIR3DL1 allele groups *005 and *007) bind to HLA-Bw4 with T80 to confer a strong inhibitory signal. In a retrospective cohort of 299 patients undergoing allo HCT for AML, we demonstrated that these highly inhibitory donor KIR3DL1/recipient HLA-Bw combinations (KIR3DL1-HIGH) resulted in a greater incidence of recipient relapse when compared to other donor/recipient KIR3DL1/HLA-Bw pairings with low or absent inhibitory signal (KIR3DL1-LOW/NO). (Giglio F et al, ASH Annual Meeting Abstracts, 2012) Here, we evaluated whether it was feasible to prospectively type and use KIR3DL1 allotypes in unrelated allo HCT donor selection, and whether this intervention would result in improved outcomes in patients undergoing transplant for AML and MDS. We performed PCR-SSP based intermediate resolution KIR3DL1 allele typing on all unrelated adult donors evaluated for patients with MDS and AML at our center from 2013 to present as previously described. (Boudreau J et al, PLoS One, 2014) KIR3DL1 status was provided to the treating physicians, who made the final donor selection. A total of 941 prospective allo HCT donors underwent high resolution HLA typing and KIR3DL1 allotyping for 252 patients (median per patient = 4, range 1-12). Among all donors evaluated, 27% were found to be KIR3DL1-HIGH when considering the respective recipient HLA-Bw. Having multiple donors evaluated improved the likelihood of avoiding a KIR3DL1-HIGH donor: Among recipients with one donor evaluated, 27% had only KIR3DL1-HIGH donors available compared to 12% in recipients with 2-3 donors evaluated and 4% for recipients with >3 donors evaluated (P < 0.0001). Among all evaluated patients, 41% had both KIR3DL1-HIGH and KIR3DL1-LOW/NO donors available, indicating a potential selection based on KIR3DL1 was possible. Among 252 patients evaluated, 115 proceeded to allo HCT (48 with MDS, 67 with AML). The median age at transplant was 62 years (range 3.6-78). Donors were HLA matched in 105 transplants and were single loci mismatched in 10 transplants. Conditioning was myeloablative in 73 (11 with total body irradiation). GVHD prophylaxis was with ex vivo CD34+ selection in 65 patients and with tacrolimus/methotrexate in the remaining patients. The median follow-up in transplanted patients was 13.1 months (range 0.5-43.3 months). On univariate analysis, the 2-year disease-free survival was 64% (95% confidence interval: 54-76%) in those with KIR3DL1-LOW/NO donors versus 39% (22-68%) in recipients with KIR3DL1-HIGH donors (P = 0.05). The incidence of relapse was similar but favored patients with KIR3DL1-LOW/NO donors (26% [15-37%] versus 35% [13-57%], P = 0.5). 2-year overall survival was similar between those with KIR3DL1-LOW/NO versus KIR3DL1-HIGH donors (75% [65-86%] versus 69% [52-91%], P = 0.43). The time from the initiation of a formalized donor search to transplant did not differ between recipients with KIR3DL1-LOW/NO versus KIR3DL1-HIGH donors (median 81 v. 83 days, respectively, P = 0.97). Recipients with KIR3DL1-LOW/NO donors were CIBMTR Transplant Risk Score low = 53, intermediate = 6, and high = 33; whereas recipients of KIR3DL1-HIGH donors were low = 17, intermediate = 2, and high = 4 (P = 0.15). These results indicate that disease severity and transplant urgency did not influence whether a KIR3DL1-LOW/NO donor was able to be selected. In summary, these prospective data on 115 patients from a single center support improved outcomes in patients with AML and MDS undergoing unrelated donor allo HCT using a donor with low or absent KIR3DL1 inhibition. A multi-center, prospective study to evaluate the prospective use of HLA and KIR genotype based selection of URDs for patients undergoing allo HCT for AML is underway (NCT02450708). Figure 1. Figure 1. Figure 2. Figure 2. Disclosures Kernan: Gentium: Research Funding; The National Cancer Institute of the National Institutes of Health: Research Funding.

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47

Steiniger, B., J. Klempnauer, E. Günther, and K. Wonigeit. "Detection of polymorphic rat MHC antigen determinants in cryostat sections. A method for selecting monoclonal alloantibodies." Journal of Histochemistry & Cytochemistry 34, no. 8 (August 1986): 1105–8. http://dx.doi.org/10.1177/34.8.2426336.

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An immunohistological method for detection of rat MHC antigens by unconjugated primary alloantibodies is described. The procedure is based on secondary reagents specific for an allotypic marker of rat kappa light chains and makes possible differentiation between specifically bound alloantibody and the ubiquitously distributed interstitial immunoglobulin in the section. This technique can be used to pre-select monoclonal antibodies to be coupled to biotin or enzymes for histological application.

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48

Imanishi-Kari, T., C. A. Huang, J. Iacomini, and N. Yannoutsos. "Endogenous Ig production in mu transgenic mice. II. Anti-Ig reactivity and apparent double allotype expression." Journal of Immunology 150, no. 8 (April 15, 1993): 3327–46. http://dx.doi.org/10.4049/jimmunol.150.8.3327.

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Abstract In 17.2.25 mu transgenic mice (M54, M95), many of the expressed Ig, whether encoded by the transgene or endogenous H chain genes, react with Ig. IgM antibodies encoded by the 17.2.25 mu transgene transfected into J558L myeloma cells are also Ig reactive. In addition, anti-Ig reactivity was manifested by antibodies of the IgM, IgG, and IgA isotypes from the transgenic mice, suggesting that this characteristic reactivity is associated with VH and VL domains of these antibodies. These antibodies bind the (Fab')2 fragment of mouse IgG1 mAb known to be directed against C mu allotypic determinants. This finding could account for the so called "double producer" B cells found in mu transgenic mice and previously identified in serologic assays conducted with two different anti-mu allotypic reagents. In transgenic mice, a high frequency of the antibodies encoded by the transgene or endogenous H chain genes react with polyclonal and monoclonal antiidiotypic antibodies raised against the 17.2.25 Id. The idiotypic and/or antiidiotypic reactivity displayed by antibodies derived from these transgenic mice is similar to that of antibodies expressed by neonatal B cells of normal mice. Thus, our data suggest that transgene expression can play an important role in shaping the endogenous repertoire of antibody specificities.

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49

Velez, Maria-Gabriela, Melissa Kane, Sucai Liu, Stephen B. Gauld, John C. Cambier, Raul M. Torres, and Roberta Pelanda. "Ig Allotypic Inclusion Does Not Prevent B Cell Development or Response." Journal of Immunology 179, no. 2 (July 3, 2007): 1049–57. http://dx.doi.org/10.4049/jimmunol.179.2.1049.

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50

Butler, John E., Nancy Wertz, Nick Deschacht, Serge Muyldermans та Joan K. Lunney. "Eleven porcine C gamma (Cγ) genes: Phylogeny, expression and allotypic variants". Veterinary Immunology and Immunopathology 128, № 1-3 (березень 2009): 311–12. http://dx.doi.org/10.1016/j.vetimm.2008.10.217.

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