179.Goossens D., Champomier F., Rouger P., Salmon C. Human monoclonal antibodies against bloodgroupantigens:preparationofaseriesofstableEBVimmortalizedBclonesproducing high levels of antibody of different isotypes and specificities // J. Immunol. Methods. – 1987. – V. 101. – P. 193–200.
180.Gordon M.C., Kennedy M.S., O’Shaughnessy R.W., Waheed A. Severe hemolytic disease of the newborn due to anti-Js b // Vox Sang. – 1995. – V. 69. – P. 140–141.
181.GorlinJ.B.,KellyL.AlloimmunisationviaprevioustransfusionplacesfemaleKp b-negative recipients at risk for having children with clinically significant hemolytic disease of the newborn // Vox Sang. – 1994. – V. 66. – P. 46–8.
182.Grant S.R., Kilby M.D., Meer L. et al. The outcome of pregnancy in Kell alloimmunisation // Brit.J.Obstet.Gynec.–2000.–V.107.–P.481–485.
183.Greenwalt T.J., Walker R.H., Argall C.I. et al. Js b of the Sutter blood group system // Proc. 9-th Congr. int. Soc. Blood Transf. – Mexico, 1962. – P. 235–237.
184.Grove-Rasmussen M., Huggins C.E. Selected types of frozen blood for patients with multiple blood group antibodies // Transfusion. – 1973. – V. 13. – P. 124.
185.Guevin R.M., Taliano V., Waldmann O. The Cote serum (anti-K11), an antibody defining a new in variant the Kell system // Vox Sang. – 1976. – V. 31 (Suppl. 1). – P. 96–100.
186.Guevin R.M., Taliario V., Waldmann O. The Cote serum, an antibody defining a new variant in theKellsystem//Amer.Ass.BloodBanks,Program:24-thAnnualMeeting,1971.–P.100.
187.Hamilton H.B., Nakahara Y. The rare Kell blood group phenotype K° in a Japanese family
//Vox Sang. – 1971. – V. 20. – P. 24–28.
188.Hanaoka N., Yoshida K., Nakamura A. et al. A novel frameshift mutation in the McLeod syndrome gene in a Japanese family // J. Neurol. Sci. – 1999. –V. 165. – P. 6–9.
189.Hardie R.J., Pullon H.W. H., Harding A.E. et al. Neuroacanthocytosis: a clinical, haematological and pathological study of 19 cases // Brain. – 1991. – V. 114. – P. 13–49.
190.Hardman J.T., Beck M.L. Hemagglutination in capillaries: correlation with blood group specificity and IgG subclass // Transfusion. – 1981. – V. 21. – P. 343–346.
191.HardyJ.,NapierJ.A.RedcellantibodiesdetectedinantenataltestsonRhesuspositivewoman in south and midWales 1948–1978 // Brit. J. Obstet. Gynaec. – 1981. –V. 88. – P. 91–100.
192.Hare V., Wilson M.J., Wilkinson S., Issitt P.D. A Kell system antibody with highly unusual characteristics [Abstract] // Transfusion. – 1981. – V. 21. – P. 613.
193.Harrison J. The ‘naturally occurring’anti-E // Vox Sang. – 1970. – V. 19. – P. 123.
194.Hawley W.C., Blanda E., Kennedy M.S. (abstract) // Transfusion. – 1975. – V. 15. – P. 521.
195.Heisto H., Guevin R. M., Taliano V. et al. Three further antigen-antibody specificities associated with the Kell blood group system // Vox Sang. – 1973. – V. 24. – P. 179–180.
196.Hessner M.J., McFarland J G., Endean D.J. Genotyping of KEL1 and KEL2 of the human Kell gene blood group system by the polymerase chain reaction with sequence-specific primers //Transfusion. – 1996. –V. 36. – P. 495–499.
197.Heyworth P.G., Curnutte J.T., Rae J. et al. Hematologically important mutations: X-linked chronic granulomatous disease (second update) // Blood Cells Mol. Dis. – 2001. – V. 27. – P. 16–26.
198.Ho M., Chelly J., Carter N. et al. Isolation of the gene for McLeod syndrome that encodes a novel membrane transport protein // Cell. – 1994. – V. 77. – P. 869–880.
199.HoM.E.,ChalmersR.M.,DavisM.B.etal.AnovelpointmutationintheMcLeodsyndrome gene in neuroacanthocytosis //Ann. Neurol. – 1996. – V. 39. – P. 672–675.
200.Ho M.F., Monaco A.P., Blonden L.A. J. et al. Fine mapping of the McLeod locus (XK) to a 150–380 kb region in Xp21 //Amer. J. Hum. Genet. – 1992. – V. 50. – P. 317–330.
201.Hughes-Jones N.C., Gardner B.The Kell system studied with radioactively-labelled anti-K
//Vox Sang. – 1971. – V. 21. – P. 154–158.
202.Inglis G., Fraser R.H., McTaggart S. et al. Monoclonal antibodies to high incidence Kell epitopes: characterization and application in automated screening of donor samples // Transfus. Med. – 1994. – V. 4. – P. 209–212.
436
203.Issitt P.D. On the incidence of second antibody populations in the sera of women who have developed anti-Rh antibodies // Transfusion. – 1965. – V. 5. – P. 355.
204.Issitt P.D., Anstee D.J. Applied Blood Group Serology. – 4-th ed. – Durham, NC, USA: Montgomery Sc. Publ., 1998. – P. 609–653.
205.Issitt P.D., Combs M.R., Bredenhoeft S.J. et al. Lack of clinical significance of «enzymeonly» red cell alloantibodies // Transfusion. – 1993. – V. 33. – P. 284–293.
206.Issitt P.D., Combs M.R., Bumgarner D.J. et al. Studies of antibodies in the sera of patients who have made red cell autoantibodies // Transfusion. – 1996. – V. 36. – P. 481–486.
207.Issitt P.D., McKeever B.G., Moore V.K., Wilkinson S.L. Three examples of Rh-positive, good responders to blood group antigens // Transfusion. – 1973. – V. 13. – P. 316.
208.Issitt P.D., PavoneB.G. Criticalre-examinationof thespecificityof auto-anti-Rhantibodies in patients with a positive direct antiglobulin test // Brit. J. Haemat. – 1978. –V. 38. – P. 63.
209.Ito K., Mukumoto Y., Konishi H. An example of ‘naturally occurring’ anti-Js a (K6) in a Japanese female // Vox Sang. – 1979. – V. 37. – P. 350–351.
210.Jaber A., Blanchard D., Goossens D. et al. Characterization of blood group Kell (K1) antigenwithahumanmonoclonalantibody//Blood.–1989.–V.73.–N6.–P.1597–1602.
211.Jaber A., Loirat M., Willem C. et al. Characterization of murine monoclonal antibodies directed against the Kell blood group glycoprotein // Brit. J. Haemat. – 1991. – V. 79. –
P.311–315.
212.Jarkowski T.L., Hinshaw C.P., Beattie K.M., Silberberg B. Another example of anti-Js a // Transfusion. – 1962. – V. 2. – P. 423.
213.Jones J., Reid M.E., Oyen R. et al. A novel common Kell antigen, TOU, and its spatial relationship to other Kell antigens // Vox Sang. – 1995. – V. 69. – P. 53–60.
214.Jongeneel C.V., Bouvier J., Bairoch A. A unique signature identifies a family of zincdependent metallopeptidases // FEBS Lett. – 1989. – V. 242. – P. 211–214.
215.Jongerius J.M., Daniels G.L., Overbeeke M.A.M. et al.Anew low-incidence antigen in the Kell blood group system VLAN (KEL25) // Vox Sang. – 1996. – V. 71. – P. 43–47.
216.Judd W.J. Methods in Immunohematology // Montgomery Scientific Publications. – 2-nd. – 1994. – 476 p.
217.Judd W.J., Walter W J., Steiner E.A. Clinical and laboratory findings on two patients with naturally occurring anti-Kell agglutinins // Transfusion. – 1981. – V. 21. – P. 184–188.
218.Judson P.A., Anstee D.J. Comparative effect of trypsin and chymotrypsin on blood group antigens // Med. Lab. Sci. – 1977. – V. 34. – P. 1–6.
219.Jung H.H., Hergersberg M., Kneifel S. et al. McLeod syndrome: a novel mutation, predominant psychiatric manifestations, and distinct striatal imaging findings // Ann. Neurol. – 2001. – V. 49. – P. 384–392.
220.KaitaH.,LewisM.,ChownB.,CardE.AfurtherexampleoftheKellbloodgroupphenotype K −, k −, Kp(a −b −) // Nature. – 1959. – V. 183. – P. 1586.
221.Kanel G.C., Davis I., Bowman J.E. ‘Naturally-occurring’anti-K1: possible association with mycobacterium infection // Transfusion. – 1978. – V. 18. – N 4. – P. 472–473.
222.Kawakami T., Takiyami Y., Sakoe K. et al. A case of McLeod syndrome with unusually severe myopathy // J. Neuro. Sci. – 1999. – V. 166. – P. 36–39.
223.Kelley C.M., Karwal M.W., Schlueter A.J., Olson J.D. Outcome of transfusion of K:11 erythrocytes in a patient with anti-K11 antibody // Vox Sang. – 1998 – V. 74. – P. 205–208.
224.Khamlichi S., Bailly P., Blanchard D. et al. Purification and partial characterization of the erythrocyte Kx protein deficient in McLeod patients // Eur. J. Biochem. – 1995. –
V.228. – P. 931–934.
225.Kikuchi M., Endo N., Seno T. et al.AJapanese family with two Kp(a −b −c + ) members, pre sumed genotype Kp c / K° // Transfusion.. – 1983. – V. 23. – P. 254–255.
226.Kline W.E., Sullivan C.M., Bowman R.J.Arare example of weakened expression of the Kell (K1) antigen // Vox Sang. – 1984. – V. 47. – P. 170–173.
437
227.KlugeA., Jungfer H.Anti-K2 (Cellano) blood group antibodies: typing as IgG and IgAwith a review of their clinical significance // Blut. – 1970. – V. 21. – P. 357–365.
228.Kohan A.I., Reybaud J.F., Salamone H.J. et al. Management of a severe transfusional problem in a patient with alloantibody to Kp b (K4) // Vox Sang. – 1990. – V. 59. –
P.216–217.
229.Kornstad L., Heistö H. The frequency of formation of Kell antibodies in recipients of Kellpositive blood // Proc. 6-th Congr. Europ. Soc. Haemat. – Copenhagen, 1957. – P. 754.
230.KuypersF.A.,vanLinde-SibeniusTripM.,RoelofsenB.etal.Thephospholipidorganisation in the membranes of McLeod and Leach phenotype erythrocytes // FEBS Lett. – 1985. –
V.184. – P. 20–44.
231.Lee S. Molecular basis of Kell blood group phenotypes // Vox Sang. – 1997. – V. 73. –
P.1–11 and Vox Sang. – 1998. – V. 74. – P. 58.
232.Lee S., Bennett P.R., Overton T. et al. Prenatal diagnosis of Kell blood group genotypes: KEL1 and KEL2 //Amer. J. Obstet. Gynecol. – 1996. – V. 175. – P. 455–459.
233.Lee S., Lin M., Mele A. et al. Proteolytic processing of big endothelin–3 by the Kell blood group protein // Blood.– 1999. – V. 94. – P. 1440–1450.
234.Lee S., Naime D., Reid M., Redman C. The KEL24 and KEL24 alleles of the Kell blood group system // Transfusion. – 1997. – V. 37. – P.1035–1038.
235.Lee S., Reid M.E., Redman C.M. Point mutations in KEL exon 8 determine a high-incidence (RAZ) and a low-incidence (KEL25, VLAN) antigen of the Kell blood group system // Vox Sang.–2001.–V.81.–P.259–263.
236.Lee S., Russo D.C.W., Pu J. et al. The mouse Kell blood group gene (Kel): cDNA sequence, genomicorganization,expression,andenzymaticfunction//Immunogenetics.–2000.–V.52.–
P.53–62.
237.Lee S., Russo D.C., Reid M., Redman C. Mutations that diminish expression of Kell
surface protein and lead to the Kmod RBC phenotype // Transfusion. – 2003. – V. 43. – N 8. – P. 1121–1225.
238.Lee S., Russo D.C.W., Reiner A.P. et al. Molecular defects underlying the Kell null phenotype // J. Biol. Chem. – 2001. – V. 276. – P. 27281–2729.
239.Lee S., Wu X., Reid M. et al. Molecular basis of the Kell (Kl) phenotype // Blood. – 1995. –
V.85. – P. 912–916.
240.Lee S., Wu X., Reid M., Redman C. Molecular basis of the K:6,–7 [Js(a +b −)] phenotype in the Kell blood groups system // Transfusion. – 1995. – V. 35. – P. 822–825.
241.LeeS.,WuX.,SonS.etal.PointmutationscharacterizeKEL10,theKEL3,KEL4,andKEL21 alleles, and the KEL17 and KEL11 alleles //Transfusion. – 1996. –V. 36. – P. 490–494.
242.LeeS.,ZambasE.D.,GreenE.D.,RedmanC.Organizationofthegeneencodingthehuman Kell blood group protein // Blood. – 1995. – V. 85. – P. 1364–1370.
243.Lee S., Zambas E.D., Marsh W.L., Redman C.M. Molecular cloning and primary structure of Kell blood group protein // Proc. Nat.Acad. Sci. USA. – 1991. – V. 88. – P. 6353–6357.
244.Lee S., Zambas E.D., Marsh W.L., Redman C.M. The human Kell blood group gene maps to chromosome 7q33 and its expression is restricted to erythroid cells // Blood. – 1993. –
V.81. – P. 2804–2809.
245.Leggat H.M., Gibson J.M., Barren S.L., Reid M.M.Anti-Kell in pregnancy // Brit. J. Obstet. Gynec. – 1991. – V. 98. – P. 162–165.
246.Levene C., Rudolphson Y., Shechter Y. A second case of hemolytic disease of the newborn due to anti-Js a // Transfusion. – 1980. – V. 20. – P. 714–715.
247.Levene C., Sela R., DaCosta Y., Manny N. Clinical significant of anti-K22 [Abstract]. 20th Congr // Int. Soc. Blood. Transfus. – 1988. – P. 295.
248.Levine P. The influence of the ABO system on hemolytic disease // Hum. Biol. – 1958. –
V.30. – P. 14.
249.Lewine P., Backer M., Wigod M., Ponder R. A new human hereditary blood property (Cellano) present in 99,8 % of all bloods // Science. – 1949. – V. 109. – P. 464–467.
438
250.Lewis M, Chown B, Kaita H. Inheritance of blood group antigens in a largely Eskimo population sample //Amer. J. Hum. Gene. – 1963. – V. 15. – P. 203–208.
251.Lewis M., Kaita H., Chown B. The inheritance of the Kell blood groups in a Caucasian population sample // Vox Sang. – 1969. – V. 17. – P. 221–223.
252.Lewis M., Kaita H., Duncan D., Chown B. Failure to find hypothetic K a (KKp a) of the Kell blood group system // Vox Sang. – 1960. – V. 5. – P. 565–567.
253.Lombardo J.M., Britton S.J., Hannon G., Terry D. Kо in a sister and brother, a family study
//AbstractsAABB and ISH Meeting. –Washington, 1972. – P. 59.
254.Longster G.H., Major K.E. Anti-K (K1) in ascitic fiuid // Vox Sang. – 1975. – V. 28. –
P.253.
255.Lowe R.F., MusengeziA.T, Moores P. Severe hemolytic disease of the newborn associated with anti-Js b // Transfusion. – 1978. – V. 18. – P. 466–468.
256.Manny N., Levene C., Harel N. et al. The second example of anti-K22 and a family genetically informative for and K22 // Vox Sang. – 1985. – V. 49. – P. 135–137.
257.Manny N., Levene C., Sela R. et al.Autoimmunity and the Kell blood groups: auto-anti-Kp b in a Kp(a +b −) patient // Vox Sang. – 1983. – V. 45. – P. 252–256.
258.Marsh W.L. Letter // Vox Sang. – 1979. – V. 36. – P. 375–376.
259.Marsh W.L., Marsh N.J., MooreA. et al. Elevated serum creatine phosphokinase in subjects with MacLeod syndrome // Vox Sang. – 1981. – V. 40. – P. 403–411.
260.Marsh W.L., DiNapoli J., Qyen R. et al. Delayed hemolytic transfusion reaction caused by the second example of anti-K19 // Transfusion. – 1979. – V. 19. – P. 604–608.
261.Marsh W.L., DiNapoli J., Qyen R.Auto-immune hemolytic anemia caused by anti-K13 // Vox Sang.–1979.–V.36.–P.174–178.
262.Marsh W.L., Jensen L., Oyen R. et al. Anti-K13 and the K:-13 phenotype: a blood-group variant related to the Kell system // Vox Sang. – 1974. – V. 26. – P. 34–40.
263.Marsh W.L., Mueller K.A., Johnson C.L. Use of AET-treated cells in the investigation of Kell related autoimmunity [Abstract] // Transfusion. – 1982. – V. 22. – P. 419.
264.Marsh W.L., Nichols M.E., Qyen R. et al. Naturally occurring anti-Kell stimulated by E. coli enterocolitis in a 20-day-old child // Transfusion. – 1978. – V. 18. – P. 149–154.
265.Marsh W.L., Qyen R., Alicea E. et al. Autoimmune hemolytic anemia and the Kell blood groups //Amer. J. Hematol. – 1979. – V. 7. – P. 155–162.
266.Marsh W.L., Qyen R., Nichols M.E. Kx antigen, the McLeod phenotype, and chronic granulomatous disease: further studies // Vox Sang. – 1976. – V. 31. – P. 356–362.
267.Marsh W.L., Qyen R., Nichols M.E.,Allen F.H. Chronic granulomatous disease and the Kell blood groups // Brit. J. Haemat. – 1975. – V. 29. – P. 247–262.
268.Marsh W.L., Redman C.M. Recent developments in the Kell blood group system // Transfusion Med. Rev. – 1987. – V. 1. – P. 4–20.
269.Marsh W.L., Redman C.M. The Kell blood group system: a review // Transfusion. – 1990. –
V.30. – P. 158–167.
270.Marsh W.L., Redman C.M., Kessler L.A. et al. K23: a low-incidence antigen in the Kell blood group system identified by biochemical characterization // Transfusion. – 1987. –
V.27. – P. 36–40.
271.Marsh W.L., Schnipper E.F., Johnson C.L. et al.An individual with McLeod syndrome and the Kell blood group antigen K (K1) // Transfusion. – 1983. – V. 23. – P. 336–338.
272.Marsh W.L., Stroup M., Macilroy M. et al. A new antibody, anti-K12, associated with the Kell blood group system // Vox Sang. – 1973. – V. 24. – P. 200–205.
273.Marsh W.L., Taswell M.F., Oyen R. et al. Kx antigen of the Kell system and its relationship to chronic granulomatous disease. Evidence that the Kx gene is X-linked // Transfusion. – 1975. – V. 15. – N 3. – P. 527.
274.Mastroberardino L., Spindler B., Pfeiffer R. et al.Amino-acid transport by heterodimers of 4F2hc / CD98andmembersofthepermeasefamily//Nature.–1998.–V.395.–P.288–291.
439
275.MazzaraR.,LozanoM.,SalmeronJ.M.etal.TransfusionofincompatibleRBCstoapatient with alloanti-Kp b // Transfusion. – 2001. – V. 41. – P. 611–614.
276.McDowell M.A., Mann J.M., Milakovic K. Kell-like antibody in a Kell positive patient [Abstract] // Transfusion. – 1978. –V. 18. – P. 389.
277.McGinniss M.H., Dean A. Expression of red cell antigens by K562 human leukemia cells before and after induction of hemoglobin synthesis by hemin // Transfusion. – 1985. –
V.25. – P. 105–109.
278.McGinniss M.H., MacLowry J.D., Holland P.V. Acquisition of K1-like antigen during terminal sepsis // Transfusion. – 1984. – V. 24. – P. 28–30.
279.McKennaD.S.,NagarajaH.N.,O’ShaughnessyR.Managementofpregnanciescomplicated by anti-Kell isoimmunization // Obstet. Gynecol. – 1999. – V. 93. – P. 667–673.
280.McNeil C., Newman M. Неопубликованное сообщение, 1966. Цит. по Race R. R., Sanger
R.Blood Groups in Man. – 6-th ed. –Oxford: BSP, 1975. – P. 303.
281.Merry A.H., Thomson E.E., Anstee D.J., Stratton F. The quantification of erythrocyte antigen sites with monoclonal antibodies // Immunology. – 1984. – V. 51. – P.793–800.
282.Merry A.H., Thomson E.E., Lagar J. et al. Quantitation of antibody binding to erythrocytes in LISS // Vox Sang. – 1984. – V. 47. – P. 125–132.
283.MifsudN.A.,HaddadA.P.,SparrowR.L.,CondonJ.A.Useofthepolymerasechainreactionsequence specific oligonucleotide technique for the detection of the K1 / K2 polymorphism of the Kell blood groups system // Blood. – 1997. – V. 89. – P. 4662–4663.
284.Mollison P.L., Engelfriet C.P., Contreras M. Blood Transfusion in Clinical Medicine. – 10-th ed. – Oxford: BSP, 1997. – 1033 p.
285.Molthan L., Strohm P.L. Hemolytic transfusion reaction due to anti-Kell undetectable in low- ionicstrengthsolutions//Amer.J.Clin.Path.–1981.–V.75.–P.629–631.
286.Moore S.B., Taswell H.F., Pineda A.A. Delayed hemolytic transfusion reactions. Evidence of the need for an improved pretransfusion compatibility test //Amer. J. Clin. Path. – 1980. – V. 74. –
P.94–97.
287.MorganP.,BossomE.L.‘Naturallyoccurring’anti-Kell(K1):twoexamples//Transfusion.– 1963. – V. 3. – P. 397–398.
288.Morton N.E., Krieger H., Steinberg A. G., Rosenfield R.E. Genetic evidence confirming the localization of Sutter in the Kell blood-group system // Vox Sang. – 1965. –V. 10. –
P.608–613.
289.Moulds J.J., Moulds M.K. Inactivation of Kell blood group antigens by 2-aminoethylisothiouronium bromide // Transfusion. – 1983. – V. 23. – P. 274–275.
290.MourantA.E.,KopecA.C.,Domaniewska-SobczakK.TheDistributionoftheHumanBlood Groups and Other Polymorphisms, 2-nd ed. – London: Oxford University Press, 1976.
291.Mukumoto Y., Konishi H., Ito K. et al.An example of naturally occurring anti-Kell (K1) in a Japanese male // Vox Sang. – 1978. – V. 35. – P. 275–276.
292.Muller A., Andre-Liardet J., Garretta M. et al. Observations sur un anticorps rare. 1’antiGerbich // Rev Franc Transfus. –1973. – V. 16. – P. 251–257.
293.Mullis N. C., Harris D. F., Roberts C. et al. Intravascular hemolysis caused by anti-K2 [Abstract] // Transfusion. – 1999. – V. 39 (Suppl.). – P. 475.
294.Murphy M.T., Fraser R.H., Goddard J.P. Development of a PCR-based diagnostic assay for the determination of KEL genotype in donor blood samples // Transfus. Med. – 1996. –V. 6. – P. 133–137.
295.Murphy M.T., Morrison N., Miles J. S. et al. Regional chromosome assigment of the Kell blood group locus (KEL) to chromosome 7q33-q35 by fluorescence in situ hybridization: evidence for the polypeptide nature of antigenic variation // Hum. Genet. – 1993. – V. 91. –
P.585–588.
440