ABSTRACT
ItisofinteresttonotethatsometimesonlysomeoftheRBCsareaffected,suggestingan abnormalcloneofcells(418,424,425).Rentonetal.(426)describedafascinatingexampleof this.AgroupA1BleukemicpatientlostallA1antigenicactivity.Rentonetal.wereableto separateAB,A,B.and0cellsfromthepatient'sblood.Theproportionswereasfollows:20% 0,12%A,42%B,and20%AB.Itwasthoughtthatthe0cellswereproducedastheresult oftwoindependentprocesses(i.e.,lossofAandB),suggestingthatthealterationwasata
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Figure3ReactionsofgroupARBCs,frompatientswithvarioushematologicalconditions,with anti-At.Themeanagglutinationscoresandnormalrangeareintheboxontherightsideofthefigure. AnyscoresontheleftsideofthisboxindicatereducedAantigenstatusofRBCs.(FromRef.422.)
DoBloodGroupsHaveaBiologicalRole229
chromosomallevel.Rentonetal.(426)andothers(427)haveshownthatnormalRBCs transfusedintosuchpatientsretainanintactAantigen,whereasthepatients'owncellscontinue toundergomodification.DepressionsofABHantigenshavebeennotedinpregnancy(428) andonrareoccasionsinnormalindividuals(particularlytheaged).Salmon(421)describesa caseofanelderlywoman(70yearswhenfirstseen)whowashematologicallynormal,witha dualpopulationofRBCs,50%ofthehematopoietictissuebeingunabletoproduceA1antigen. TheseRBCswereshownalsotohaveadeficiencyoftheRBCenzymeadenylatekinase1 (AK1).ItisknownthattheAKIlocusisclosetotheABOlocusonthelongarmofchromosome 9at9q34.Itwassuggestedthatinonecloneofcellsintheseindividuals,theportionof chromosome9carryingABOandAKJisaffected(418,421).Apatientwitherythroleukemia withweakenedAantigensandAKIdeficiencyhasalsobeendescribed(429).
