Neutrophil-specific antigen HNA-2a, NB1 glycoprotein, and CD177

Current Opinion in Hematology

Volumn 14, Issue 6, 2007, Pages 688-693

  Stroncek, David F ^a,b  

^a NATIONAL INSTITUTES OF HEALTH   (United States)

^b NATIONAL INSTITUTES OF HEALTH   (United States)

Author keywords

CD177; HNA 2a; NB1; Neutrophil antigens; PRV 1

Indexed keywords

ANTIGEN; BIOLOGICAL MARKER; CD31 ANTIGEN; GLYCOPROTEIN; HUMAN NEUTROPHIL ANTIGEN 2A; JANUS KINASE 2; MESSENGER RNA; MYELOBLASTIN; UNCLASSIFIED DRUG;

BLOOD TRANSFUSION; BLOOD TRANSFUSION REACTION; CELL MEMBRANE; GENE MUTATION; GENE OVEREXPRESSION; HUMAN; LEUKOCYTE ACTIVATION; MYELOPROLIFERATIVE DISORDER; PRIORITY JOURNAL; PROTEIN EXPRESSION; PROTEIN LOCALIZATION; REVIEW; RISK ASSESSMENT; WEGENER GRANULOMATOSIS;

ANTIGENS, CD31; ANTIGENS, SURFACE; BIOLOGICAL MARKERS; BLOOD TRANSFUSION; CELL MEMBRANE; HUMANS; ISOANTIGENS; MEMBRANE GLYCOPROTEINS; NEUTROPHILS; POLYCYTHEMIA VERA; RECEPTORS, CELL SURFACE; THROMBOCYTHEMIA, HEMORRHAGIC; WEGENER GRANULOMATOSIS;

EID: 34848904867     PISSN: 10656251     EISSN: 15317048     Source Type: Journal    
DOI: 10.1097/MOH.0b013e3282efed9e     Document Type: Review

References (48)

1. Stroncek DF, Skubitz KM, McCullough JJ. Biochemical characterization of the neutrophil-specific antigen NB1. Blood 1990; 75:744-755.
2. Kissel K, Santoso S, Hofmann C, et al. Molecular basis of the neutrophil glycoprotein NB1 (CD177) involved in the pathogenesis of immune neutropenias and transfusion reactions. Eur J Immunol 2001; 31:1301-1309.
3. Temerinac S, Klippel S, Strunck E, et al. Cloning of PRV-1, a novel member of the uPAR receptor superfamily, which is overexpressed in polycythemia rubra vera. Blood 2000; 95:2569-2576.
4. Caruccio L, Bettinotti M, Director-Myska AE, et al. The gene overexpressed in polycythemia rubra vera, PRV-1, and the gene encoding a neutrophil alloantigen, NB1, are alleles of a single gene, CD177, in chromosome band 19q13.31. Transfusion 2006; 46:441-447. This study showed that PRV-1 and NB1 are alleles of the gene CD177.
5. Matsuo K, Lin A, Procter JL, et al. Variations in the expression of granulocyte antigen NB1. Transfusion 2000; 40:654-662.
6. Caruccio L, Bettinotti M, Matsuo K, et al. Expression of human neutrophil antigen-2a (NB1) is increased in pregnancy. Transfusion 2003; 43:357-363.
7. Caruccio L, Walkovich K, Bettinotti M, et al. CD177 polymorphisms: correlation between high-frequency single nucleotide polymorphisms and neutrophil surface protein expression. Transfusion 2004; 44:77-82.
8. Taniguchi K, Nagata H, Katsuki T, et al. Significance of human neutrophil antigen-2a (NB1) expression and neutrophil number in pregnancy. Transfusion 2004; 44:581-585.
9. Stroncek DF, Jaszcz W, Herr GP, et al. Expression of neutrophil antigens after 10 days of granulocyte-colony-stimulating factor. Transfusion 1998; 38:663-668.
10. Gohring K, Wolff J, Doppl W, et al. Neutrophil CD177 (NB1 gp, HNA-2a) expression is increased in severe bacterial infections and polycythaemia vera. Br J Haematol 2004; 126:252-254.
11. Stroncek DF, Shankar R, Litz C, Clement L. The expression of the NB1 antigen on myeloid precursors and neutrophils from children and umbilical cords. Transfus Med 1998; 8:119-123.
12. Wolff JC, Goehring K, Heckmann M, Bux J. Sex-dependent up regulation of CD 177-specific mRNA expression in cord blood due to different stimuli. Transfusion 2006; 46:132-136. Neutrophil expression of HNA-2a and CD177 mRNA is greater in neutrophils from newborns than from adults.
13. Kissel K, Scheffler S, Kerowgan M, Bux J. Molecular basis of NB1 (HNA-2a, CD177) deficiency. Blood 2002; 99:4231-4233.
14. Wolff J, Brendel C, Fink L, et al. Lack of NB1 GP (CD177/HNA-2a) gene transcription in NB1 GP- neutrophils from NB1 GP-expressing individuals and association of low expression with NB1 gene polymorphisms. Blood 2003; 102:731-733.
15. Sachs UJ, Andrei-Selmer CL, Maniar A, et al. The neutrophil specific antigen CD177 is a counter-receptor for endothelial PECAM-1 (CD31). J Biol Chem 2007; 19 June [Epub ahead of print]. This study revealed the function of NB1 glycoprotein. It is shown to bind to PECAM-1 and participates in the neutrophil transendothelial migration.
16. Kralovics R, Buser AS, Teo SS, et al. Comparison of molecular markers in a cohort of patients with chronic myeloproliferative disorders. Blood 2003; 102:1869-1871.
17. Tefferi A, Lasho TL, Wolanskyj AP, Mesa RA. Neutrophil PRV-1 expression across the chronic myeloproliferative disorders and in secondary or spurious polycythemia. Blood 2004; 103:3547-3548.
18. Sirhan S, Lasho TL, Elliott MA, Tefferi A. Neutrophil polycythemia rubra vera-1 expression in classic and atypical myeloproliferative disorders and laboratory correlates. Haematologica 2005; 90:406-408.
19. Passamonti F, Pietra D, Malabarba L, et al. Clinical significance of neutrophil CD177 mRNA expression in Ph-negative chronic myeloproliferative disorders. Br J Haematol 2004; 126:650-656.
20. Baxter EJ, Scott LM, Campbell PJ, et al. Acquired mutation of the tyrosine kinase JAK2 in human myeloproliferative disorders. Lancet 2005; 365:1054-1061.
21. James C, Ugo V, Le Couedic JP, et al. A unique clonal JAK2 mutation leading to constitutive signalling causes polycythaemia vera. Nature 2005; 434:1144-1148.
22. Kralovics R, Passamonti F, Buser AS, et al. A gain-of-function mutation of JAK2 in myeloproliferative disorders. N Engl J Med 2005; 352:1779-1790.
23. Levine RL, Wadleigh M, Cools J, et al. Activating mutation in the tyrosine kinase JAK2 in polycythemia vera, essential thrombocythemia, and myeloid metaplasia with myelofibrosis. Cancer Cell 2005; 7:387-397.
24. Zhao R, Xing S, Li Z, et al. Identification of an acquired JAK2 mutation in polycythemia vera. J Biol Chem 2005; 280:22788-22792.
25. Jones AV, Kreil S, Zoi K, et al. Widespread occurrence of the JAK2 V617F mutation in chronic myeloproliferative disorders. Blood 2005; 106:2162-2168.
26. Tefferi A, Sirhan S, Lasho TL, et al. Concomitant neutrophil JAK2 mutation screening and PRV-1 expression analysis in myeloproliferative disorders and secondary polycythaemia. Br J Haematol 2005; 131:166-171.
27. Mnjoyan Z, Yoon D, Li J, et al. The effect of the JAK2 V617F mutation on PRV-1 expression. Haematologica 2006; 91:411-412. The overexpression of CD177 (PRV-1) mRNA is due to the JAK2 V617F. Murine myeloid cells transduced with JAK2 V617F overexpressed PRV-1 mRNA but cells transduced with wild type JAK2 did not.
28. Mnjoyan Z, Li J, Afshar-Kharghan V. Expression of polycythemia rubra vera-1 decreases the dependency of cells on growth factors for proliferation. Haematologica 2005; 90:405-406.
29. Griesshammer M, Klippel S, Strunck E, et al. PRV-1 mRNA expression discriminates two types of essential thrombocythemia. Ann Hematol 2004; 83:364-370.
30. Goerttler PL, Marz E, Johansson PL, et al. Thrombotic and bleeding complications in four subpopulations of patients with essential thrombocythemia defined by c-Mpl protein expression and PRV-1 mRNA levels. Haematologica 2005; 90:851-853.
31. Johansson P, Ricksten A, Wennstrom L, et al. Increased risk for vascular complications in PRV-1 positive patients with essential thrombocythaemia. Br J Haematol 2003; 123:513-516.
32. Teofili L, Giona F, Martini M, et al. Markers of myeloproliferative diseases in childhood polycythemia vera and essential thrombocythemia. J Clin Oncol 2007; 25:1048-1053. Children with polycythemia and essential thrombocythemia have increased levels of neutrophil PRV-1 (CD177) mRNA levels and JAK V617F.
33. Steimle C, Lehmann U, Temerinac S, et al. Biomarker analysis in polycythemia vera under interferon-alpha treatment: clonality, EEC, PRV-1, and JAK2 V617F. Ann Hematol 2007; 86:239-244.
34. Samuelsson J, Hasselbalch H, Bruserud O, et al. A phase II trial of pegylated interferon alpha-2b therapy for polycythemia vera and essential thrombocythemia: feasibility, clinical and biologic effects, and impact on quality of life. Cancer 2006; 106:2397-2405. Response to interferon-α treatment of some myeloproliferative disease patients were associated with a fall in CD177 mRNA levels.
35. Passamonti F, Pietra D, Rumi E, et al. PRV-1 and its correlation with treatments and disease status in 210 patients with polycythemia vera and essential thrombocythemia. Leukemia 2005; 19:888-889.
36. Bauer S, Abdgawad M, Gunnarsson L, et al. Proteinase 3 and CD177 are expressed on the plasma membrane of the same subset of neutrophils. J Leukoc Biol 2007; 81:458-464. Proteinase 3 and NB1 glycoprotein were found to be expressed by the same subpopulation of neutrophils.
37. von Vietinghoff S, Tunnemann G, Eulenberg C, et al. NB1 mediates surface expression of the ANCA antigen proteinase 3 on human neutrophils. Blood 2007; 109:4487-4493. This study showed that the proteinase 3 and NB1 glycoprotein are co-localized on neutrophil membranes and that NB1 glycoprotein is required for the expression of proteinase 3.
38. Goldman M, Webert KE, Arnold DM, et al. Proceedings of a consensus conference: towards an understanding of TRALI. Transfus Med Rev 2005; 19:2-31.
39. Sachs UJ, Hattar K, Weissmann N, et al. Antibody-induced neutrophil activation as a trigger for transfusion-related acute lung injury in an ex vivo rat lung model. Blood 2006; 107:1217-1219. This model of neutrophil antibody-mediated transfusion related acute lung injury shows that the level of neutrophil expression of HNA-2a affects the severity of transfusion reactions due to anti-HNA-2a.
40. Silliman CC, Curtis BR, Kopko PM, et al. Donor antibodies to HNA-3a implicated in TRALI reactions prime neutrophils and cause PMN-mediated damage to human pulmonary microvascular endothelial cells in a two-event in vitro model. Blood 2007; 109:1752-1755. This model shows that neutrophil antibodies that cause transfusion related acute lung injury activate neutrophils and damage endothelial cells. The endothelial damage caused by antibody-activated neutrophils is enhanced by endotoxin treatment of the endothelial cells. This study supports the concept that multiple events are required for a transfusion to cause acute lung injury.
41. Kopko PM, Marshall CS, MacKenzie MR, et al. Transfusion-related acute lung injury: report of a clinical look-back investigation. JAMA 2002; 287:1968-1971.
42. Davoren A, Curtis BR, Shulman IA, et al. TRALI due to granulocyte-agglutinating human neutrophil antigen-3a (5b) alloantibodies in donor plasma: a report of 2 fatalities. Transfusion 2003; 43:641-645.
43. Ganguly S, Carrum G, Nizzi F, et al. Transfusion-related acute lung injury (TRALI) following allogeneic stem cell transplant for acute myeloid leukemia. Am J Hematol 2004; 75:48-51.
44. Fadeyi EA, Los Angeles MM, Wayne AS, et al. The transfusion of neutrophil-specific antibodies causes leukopenia and a broad spectrum of pulmonary reactions. Transfusion 2007; 47:545-550. This study showed that the inadvertent transfusion of anti-HNA-2a with platelet components caused leukopenia and pulmonary symptoms in a large proportion of transfusion recipients, but these recipients did not necessarily experience transfusion related acute lung injury.
45. Maslanka K, Michur H, Zupanska B, et al. Leucocyte antibodies in blood donors and a look back on recipients of their blood components. Vox Sang 2007; 92:247-249.
46. Araki N, Nose Y, Kohsaki M, et al. Antigranulocyte antibody screening with extracted granulocyte antigens by a micro-mixed passive hemagglutination method. Vox Sang 1999; 77:44-51.
47. Han TH, Chey MJ, Han KS. Granulocyte antibodies in Korean neonates with neutropenia. J Korean Med Sci 2006; 21:627-632. A solid phase mixed passive hemaglutination assay can be used to test for antibodies to HNA-1a, -1b, -2a, -4a, and -5a. Trays for testing for neutrophil antibodies can be prepared and stored frozen for several months.
48. Yasui K, Miyazaki T, Matsuyama N, et al. Establishment of cell lines stably expressing HNA-1a, -1b, and -2a antigen with low background reactivity in flow cytometric analysis. Transfusion 2007; 47:478-485.