IX. Other Blood Group Systems

Transcription

1 IX. Other Blood Group Systems A. Introduction B. I/i. In ddition to ntigens previously discussed, over 500 others cn e detected on humn rcs. 2. Antigens tht re crried y prticulr cell line of lmost ll persons re known s high-incidence or pulic ntigens. 3. Antigens crried y few individuls re clled low-incidence or privte ntigens. 4. Ech of the known ntigens descried in this lecture were initilly identified through detection of its specific ntiody in serum. 5. Knowledge of the serologic ehvior nd chrcteristics of the mjor lood group ntiodies is criticl for identifiction.. Chrcteristics of the ntiodies to lood group ntigens is very importnt when evluting pnel workups in the identifiction of irregulr ntiodies.. Considertion should e given to phse of rectivity, ntiody clss involved, nd its ility to cuse HDN nd/or hemolytic trnsfusion rections.. The I lood group system is relted to the ABO nd the Lewis systems y its iochemicl structure. 2. Antigenic development. Fetl RBCs re rich in i ntigen, nd lck I ntigen.. During the first 2 yers of life, the I ntigen grdully develops, nd there is concomitnt loss of i. c. Thus the RBCs of most dults rect strongly with nti-i while cord cells (y cells) re non-rective with nti-i. d. In rre instnces, the I ntigen never develops. These individuls, known s i dults, retin the I=i+ phenotype throughout their lives. 3. Antiodies to I/i. The unexpected ntiodies most frequently encountered when serologic test re performed t RT re those directed ginst the I nd i ntigens.. Anti-I is common cuse of non-specific gglutintion encountered t RT when performing ntiody screens, crossmtches nd my even cuse ABO discrepncies y gglutinting the reverse cells. c. Anti-I cn e detected in the serum of most norml dults if the serum is tested t 4 C. d. Anti-I is lso ssocited with typicl pneumoni cused y Mycoplsm pneumonie. Cold gglutinin titers re used to monitor their progress nd id in dignosis. MLAB IX. Other Blood Group Systems

2 e. Anti-i is clssiclly ssocited with certin virl disorders, such s infectious mononucleosis, cused y the Epstein-Brr virus, nd cytomeglovirus (CMV). 4. Clinicl Significnce. Anti-I is usully seen s enign, nturlly occurring cold\rective utontiody.. Cliniclly significnt exmples of nti-i re very rre nd occur in Cold Agglutinin Syndrome ) Antiodies re of high titer (greter thn 000). 2) Hve high therml mplitude. 3) Cuse hemolytic nemi. 4) Ptient's lood must e given through lood wrmer. c. The ntiody clss involved is IgM, so nti-i does not cuse HDN. d. Anti-I does not cuse HTRs, ut cn cuse severe utoimmune hemolytic nemi. 5. Serologicl Testing to Confirm. Test the ptient's serum ginst three group O dult cells (which re I positive), three group O cord cells (which re i positive), nd n utocontrol.. Agglutintion of the I positive dult cells nd the utocontrol long with negtive or very wek rections with the cord cells proves the presence of nti-i. c. Additionl confirmtion is otined y negtive rections when the prewrmed technique is used in the ntiody screen. Anti-I will e undetectle when the test is performed strictly t 37 C. d. In unusul cses the nti-i my e so strong tht rectivity will e otined t AHG. Autosorption or sorption using rit erythrocyte strom (REST) my hve to e done. C. The Lewis System. First identified in 946, when Mournt discovered n ntiody tht he nmed nti-le, tht he nmed fter the mker, Mrs. Lewis. Anti-Le ws discovered in 948. c d 2. Le nd Le re the mjor ntigens of the Lewis system; other ntigens in the system include Le Le, nd x Le. 3. Antigenic development. Lewis ntigens re not intrinsic to RBCs, ut re crried on plsm glycosphingolipids tht re dsored from the plsm nd inserted into the RBC memrne.. The genetic control of the two ntigens pper to reside in single gene, clled Le. Individuls who inherit t lest one Le gene will hve Lewis ntigens, individuls who re le/le (morph) will not hve Lewis ntigens. c. The Le gene cuses production of trnsferse which cuses ttchment of L-fucose to the suterminl chin of precursor chin to form the Le ntigen. IX. Other Blood Group Systems MLAB

3 d. This cn then e modified y the Lewis ctive enzyme to form Le ntigen. ) When Le is produced, it is dsored preferentilly over Le to RBC memrnes. 2) Becuse Le ntigen is produced in much greter quntities thn Le ntigens only Le cn e routinely demonstrted. e. The Lewis phenotype of RBCs depends on the phenotype of the plsm in which they re suspended nd cn e chnged y incuting the cells in plsm contining different Lewis-ctive glycolipids. ) If Le(--) RBCs re incuted with plsm contining Le or Le glycolipid, they will tke up the ntigen from the plsm. They will susequently type s positive for the Le ntigen they were incuted in. 2) If Le positive cells re incuted in plsm from n lele person, the cells will lose their Lewis ntigens nd type s Le(--). f. Lewis phenotypes nd their frequencies Whites Blcks Le(+-) 22% 23% Le(-+) 72% 55% Le(--) 6% 22% Le(++) rre rre 4. Le ntigens re sent or extremely wek t irth.. Cord lood specimens re essentilly Le(--).. Expression of the Le ntigen develops grdully, nd the infnt who is geneticlly Le(-+) my type s Le(++) during the trnsition period. c. Thus, the neworn who ppers to e Le(--) t irth cn type s Le(+-) t two months of ge, Le(++) y 2 to 8 months nd Le(-+) y 2 or 3 yers of ge. d. Lewis typing cnnot e done on ies for pternity testing. 5. Lewis ntigens during pregnncy.. Lewis ntigen strength my decline drmticlly during pregnncy.. The trnsiently Le(--) pregnnt womn my produce Lewis ntiodies during pregnncy c. These ntiodies dispper fter delivery s the norml Lewis phenotype is restored. 6. Interctions of Le, Se nd H genes.. Interctions of 3 genetic loci influence the production of the Le nd Le ntigens.. People who type s lele do not produce Le or Le ntigens, type s Le(--) nd do not hve Lewis ntigens in their plsm or secretions. But if the Se gene is present they will hve the pproprite A, B nd H sustnces in their secretions. MLAB IX. Other Blood Group Systems

4 c. Nonsecretors (genotype sese) who hve t lest one Le gene will produce only the Le() ntigen, their RBCs will type s Le(+-) nd their plsm nd secretions will contin the Le() ntigen. d. Expression of the Le(-+) phenotype depends on the presence of t lest one Le gene, one Se gene, nd one H gene. These individuls will hve oth Le nd Le ntigens in their secretions s well s the pproprite A, B, nd H sustnces in their secretions. Lewis Phenotypes nd ABH Secretions RBC Lewis Phenotype ABH Secretor Sttus Lewis Secretor Sttus Le(+-) All ABH non-secretors All secretors of Le Le(-+) All ABH secretors All secretors of Le nd Le Le(--) 7. Lewis ntiodies 80% ABH secretors 20% ABH non-secretors None. They re lmost lwys IgM nd my rect strongly t RT, even cusing ABO discrepncies if the reverse cells re positive for the pproprite Lewis ntigen.. Lewis ntiodies occur lmost exclusively in the ser of Le(--) persons, nd usully without known RBC stimulus (nturlly occurring). c. Persons whose RBC phenotype is Le(-+) do not mke nti-le ecuse smll mounts of unconverted Le re present in their sliv nd plsm. d. Anti-Le is very commonly encountered ntiody ut it is unusul to find nti-le. e. It is not unusul to find nti-le nd -Le together in the ser of Le(--) individuls. f. Most exmples of these ntiodies rect est t room temperture, ut rectivity my e seen t 37 C ut is much weker thn tht seen t RT. They lso my e detected wekly t the AHG phse if polyspecific cooms is used s the AHG regent. g. The ntiody cn ind complement nd cuse in-vitro hemolysis. Hemolysis is more often seen with enzyme treted cells. h. Becuse Lewis ntiodies do not cross the plcent nd the ntigens re poorly developed t irth, the ntiodies hve not een implicted in HDN. i. Lewis ntiodies cn e neutrlized in-vitro y the ddition of solule Lewis sustnce the ptient's serum. ) This procedure is very helpful when multiple ntiodies re suspected nd one of them is Lewis. 2) The Lewis ntiody ctivity is eliminted leving only "other" ntiody ctivity, if present. IX. Other Blood Group Systems MLAB

5 8. Trnsfusion Prctice. Lewis ntigens redily sor to nd elute from RBC memrnes. Trnsfused RBCs ssume the Lewis phenotype of the recipient within few dys of entering the circultion.. Lewis ntiodies in the recipient's serum re redily neutrlized y Lewis lood group sustnce in donor plsm. c. For these resons, it is exceedingly rre for Lewis ntiodies to cuse in-vivo hemolysis. d. It is not necessry to type donor lood for the presence or sence of Lewis ntigens prior to trnsfusion or crossmtching. ) Rections otined in the crossmtch with the donor lood provide good index of trnsfusion sfety. 2) If gglutintion nd/or hemolysis re oserved t 37 C or AHG, then the lood should not e given. D. The P Blood Group System. The P lood group system ws discovered in 927, when Lndsteiner immunized rits with humn RBCs nd used the resulting immune serums to test for ntigenic differences etween individul RBC donors.. Lndsteiner nmed the new ntigen P, ut in the following yers, s the complexity of the system egn to unfold, the terminology ws chnged.. Lndsteiner's P ntigen is now clled P, with the nme P eing ressigned to n ntigen present on lmost ll humn RBCs. 2 c. RBCs lcking P, ut shown to possess P, re of the P phenotype. 2 Phenotypes nd Frequencies Of P nd P Whites Blcks P 79% 94% 2 P 2% 6% 2 d. Other P phenotypes exist, ut re exceedingly rre (<%) nd include: P, P k, nd P k. 2. Anti-P 2. The ser of P persons commonly contin nti-p.. The ntiody rects optimlly t 4 C ut my occsionlly e detected t 37 C. c. Rrely my cuse in-vitro hemolysis. d. As it is nerly lwys IgM, it does not cross the plcent nd hs not ee reported to cuse HDN (it is poorly expressed on fetl cells). e. In generl, nti-p hs little clinicl significnce unless it is rective t 37 C. MLAB IX. Other Blood Group Systems

6 f. Anti-P hs rrely een reported to cuse hemolysis in vivo. 3. The strength of the P ntigen vries mong different RBC smples, nd ntigen strength hs een reported to diminish when RBCs re stored.. These chrcteristics sometimes cretes difficulties, oth in testing RBCs for the ntigen nd in the identifiction of the ntiody.. Anti-P lood typing regents re usully sufficiently potent to detect wek forms of the ntigen. 4. An ntiody tht is wekly rective t RT testing cn often e shown to hve nti-p specificity y lowering the incution temperture or using enzyme treted RBCs. 5. Hydtid cyst fluid or P sustnce derived form pigeon eggs inhiits the ctivity of nti-p.. Inhiition is useful id to the identifiction of nti-p, especilly if the ntiody is present in serum with multiple ntiodies.. The nti-p is neutrlized (ecomes non-rective) reveling other specificities (if present). 6. Do not hve to confirm ntigen negtive for trnsfusion. E. The MN Blood Groups. The M nd N ntigens (MNS nd MNS2 in ISBT terminology) were discovered in 927 y Lndsteiner nd Levine. 2. Studies of inheritnce indictes the genes ehve s llelic pirs tht re closely linked: MM, MN or NN. 3. Frequencies of the MN genotypes. 4. Anti-M Whites Blcks M+N- 28% 26% M+N+ 50% 44% M-N+ 22% 30%. Detected quite frequently in humn ser, usully occurring s nturlly occurring sline gglutinin in ntiody tests performed t RT.. Most exmples occur without RBC stimulus. c. Wek ntiody rectivity y nti-m cn e enhnced y lowering the ph of the test system to 6.5. d. Anti-M ser re predominntly IgM, ut rre exmples hve een found tht re prtly or wholly IgG. The M ntigen occurs in sufficient density on the RBCs tht gglutintion in sline test my occur even when the ntiody is wholly IgG. e. Rrely cliniclly significnt, lthough exmples tht rect t 37 C or AHG should e considered potentilly significnt. f. Hs rrely een ssocited with HDN or HTR. g. Do not need to confirm units re M negtive, must e crossmtch comptile. IX. Other Blood Group Systems MLAB

7 5. Anti-N. Comprtively rre.. Invrily IgM nd typiclly ehve like wekly rective cold gglutinins. c. Usully considered cliniclly insignificnt lthough some powerful nd potentilly significnt IgG exmples hve een oserved. 6. Antiodies Showing Dosge. Some individul exmples of nti-m nd nti-n demonstrte dosge, showing significntly greter rection strengths with homozygous cells thn with heterozygous cells.. Exmples of nti-m tht rect only with RBCs crrying doule dose of the M ntigen re frequently encountered. c. Anti-N showing dosge re rre encountered. d. Prolem rises due to the specificity not eing immeditely pprent from the rection ptterns otined with pnel of RBCs. 7. The M nd N ntigens re dentured when the cells re with enzymes, nd re useful in ntiody identifiction. 8. Blood grouping regents re ville from vriety of sources: humn, rit, nd monoclonl.. The most widely used lectin regent is the nti-n-like extrct of Vici grmine seeds.. Interprettion of rections with nti-m nd nti-n regents lwys requires specil cre, nd it is prticulrly importnt tht the mnufcturer's instructions e followed crefully. g 9. A very rre vrint of the MN lood group system is M. g. Person with the genotype M N will give the rections M-N+, leding to the flse conclusion tht the genotype is NN.. Of primry importnce in pternity testing. F. S, s nd U Antigens. The ntigens S (MNS3) nd s (MNS4) re produced y pir of llelic genes found t locus closely linked to the MN locus. 2. Frequencies of the S, s nd U Phenotypes Whites Blcks S+s-U+ % 3% S+s+U+ 44% 28% S-s+U+ 45% 69% S-s-U- 0 Less thn % 3. Antiodies to S, s nd U usully occur following RBC stimultion. All re considered cliniclly significnt nd cple of cusing HDN nd HTRs. MLAB IX. Other Blood Group Systems

8 . A few sline rective exmples hve een reported, ut the ntiodies re usully detected y the IAT.. Anti-S occurs out s infrequently s nti-n. c. Anti-s is seen even less often, prtly ecuse the s- phenotype is less frequently thn the S-, ut lso ecuse the ntigen is less immunogenic thn S. d. Anti-U is rre ut should e considered when serum from previously trnsfused or pregnnt Blck person contins n ntiody to high-incidence ntigen. Estlished s U negtive y proving they re S-s-. 4. S ntigen is dentured y ficin tretment, the s ntigen my or my not e dentured, depending upon the enzyme used. 5. Must confirm tht units for trnsfusion re ntigen negtive s well s crossmtch comptile. G. Luthern Blood Group System. The first exmple of nti-lu ws found in Antigens re Lu (LU) nd Lu (LU2) nd hve the following phenotypic frequencies in the white popultion: 3. Anti-Lu Lu(+-) 0.5% Lu(++) 7.5 % Lu(-+) 92.35% Lu(--) Very Rre. The ntiody is uncommon nd is usully nturlly occurring sline gglutinin.. Luthern ntigens re poorly developed t irth, nti-lu hs not een reported to cuse HDN. c. Hs not een ssocited with HTRs nd is not considered cliniclly significnt. d. My gglutinte sline suspended cells in MF mnner. This is chrcteristic of rections with some exmples of Anti-Lu. 4. Anti-Lu. Antiody production cused y exposure to ntigen through trnsfusion or pregnncy nd is considered cliniclly significnt.. Hs een reported to cuse diminished survivl of trnsfused RBCs. c. Hs een implicted in mild HDN. d. My gglutinte sline suspended cells, lthough it most commonly rects t the IAT. e. Very difficult finding ntigen negtive lood s pproximtely 99% of the popultion is ntigen positive. IX. Other Blood Group Systems MLAB 243 9

9 H. Kell Blood Group System. The K (KEL) ntigen ws first identified in 946 s the custive ntiody in cse of HDN. 2. The llele of K is Cellno, k (KEL2). 3. Phenotypes frequencies re s follows: White Blcks K+k- 0.2% Rre K+k+ 8.8% 2% K-k+ 9 % 98% 4. The Kell ntigen is strongly immunogenic, nd is frequently found in ser from trnsfused ptients. 5. Anti-K nd nti-k. Most exmples detected re of immune origin, cliniclly significnt nd re rective y the IAT, some ind complement.. Anti-K hs cused HTRs on numerous occsions, oth immedite nd delyed. c. Both hve een implicted in HDN. d. 90% of donors re K negtive, so it is not difficult finding comptile lood. e. Anti-k hs clinicl nd serologic chrcteristics similr to nti-k ut occurs much less frequently ecuse only out one person in 500 lcks the k ntigen. f. Donor units must e tested nd e negtive for the ntigen s well s crossmtch comptile. 6. Other ntigens of the Kell system.. Kp (Penney, KEL3), 957. Kp (Rutenerg, KEL4), 958 c. Js (Sutter, KEL6), 958 d. Js (Mtthews, KEL7), 963 e. K o is null phenotype. f. McLeod phenotype hs wekened expression of Kell system ntigens nd is ssocited with structurl nd functionl normlities of RBCs nd leukocytes. 7. Antiodies to other Kell system ntigens. Show similr serologic chrcteristics nd re considered cliniclly significnt.. My occur following trnsfusion or pregnncy. c. Frequency influenced y immunogenicity of the ntigen nd distriution of relevnt negtive nd positive phenotypes mong donors. d. These ntiodies re rre, suggesting tht the ntigens re of low immunogenicity. MLAB IX. Other Blood Group Systems

10 e. Ptients immunized to high incidence ntigens present prolem tht my require ssistnce from rre donor file. f. These ntiodies my cuse HDN nd HTRs. I. Duffy Blood Group System. The Fy (FY) ntigen ws discovered in the serum of multiply trnsfused hemophilic in 950. The following yer Fy (FY2) ws discovered in the serum of multiprous femle. 2. In 955 it ws reported tht most Africn Americns lcked oth the Fy nd Fy ntigens produced y wht ws thought to e codominnt lleles.. Indicted tht third llele, silent gene clled Fy (FY0) ws lso prt of the system.. Blcks who re Fy(--) re considered to e homozygous FyFy. c. The Fy(--) phenotype provides resistnce to infection with Plsmodium vivx, species of mlri. 3. Phenotypes nd frequencies of the Duffy System. Whites Blcks Fy(+-) 7% 9% Fy(++) 49% % Fy(-+) 34% 22% Fy(--) very rre 68% 4. Antiodies to Duffy ntigens.. Both nti-fy nd nti-fy cuse immedite nd delyed HTRs nd HDN. Anti-Fy is quite commonly encountered, nti-fy is considerly less common. c. The ntiodies rect est y the IAT. d. The ntigen sites re destroyed y most enzymes used in serologic tests, so nti-fy nd nti-fy ntiodies usully give negtive rections in enzyme test procedures. e. Duffy ntiodies frequently show dosge ffect, sometimes to such n extent tht they my e nonrective with heterozygous cells. f. When Duffy ntiodies re encountered it is extremely helpful to serch in the right ethnic popultion for pproprite ntigen negtive donors to crossmtch. J. The Kidd Blood Group System. Anti-Jk( ws first recognized in 95 in the serum of womn who hd given irth to child with HDN. Two yers lter, nti-jk ws found in the serum of ptient who hd suffered trnsfusion rection.. The designtion for the Kidd system is Jk (JK) nd Jk (JK2). The "null" phenotype ws discovered in 959, the individuls type s Jk(--). This is due to the silent llele Jk. More common in people of Polynesin descent. IX. Other Blood Group Systems MLAB

11 2. Phenotypes nd frequencies of the Kidd System. 3. Antiodies to Kidd Whites Blcks Jk(+=) 28% 57% Jk(++) 49% 34% Jk(=+) 23% 9% Jk(==) Exceedingly Rre. Occsionlly cuses HDN, ut it is usully mild.. These ntiodies re notorious for involvement in severe HTRs, especilly in delyed rections, which occur when ntiody, developing rpidly in n nmnestic response to ntigens on trnsfused RBCs, destroy the still circulting RBCs. ) In some reported cses, retesting the ptient's pretrnsfusion serum hs confirmed tht the ntiody ws undetectle. 2) This highlights the importnce of checking previous records prior to selecting lood for trnsfusion. In severl cses the ntiody hd een previously detected nd identified. c. Antiodies rect est y the IAT, ut sline rectivity hs een oserved. d. These ntiodies re often wekly rective nd lose rectivity upon storge, even fter freezing nd some workers feel tht RBCs crrying doule dose of Jk or Jk re needed in screening tests to relile detect these ntiodies. e. Rre exmples of Kidd ntiodies will not e detected unless fresh complement is present nd the AHG serum hs nticomplementry ctivity. ) Since these re so rre, nd due to the numer of flse positives otined when using poly cooms, it is est to use IgG. 2) Some workers report no difficulties detecting these ntiodies in low ionic tests tht incorporte nti-igg. f. Donor units must e tested with specific nti-ser nd e negtive for the ntigen s well s crossmtch comptile. K. Additionl Pirs of Antitheticl RBC Antigens. The lood group systems previously referred to re the principle ones in which the ntiodies my e frequently encountered.. Other systems of geneticlly determined ntigens lso exist nd the student should e wre of them.. These ntigens pper to e less immunogenic thn those of the other mjor lood group systems. c. Antiodies directed t these ntigens occur rrely, usully in ser contining multiple specificities nd re usully cliniclly significnt. MLAB IX. Other Blood Group Systems

12 d. The ntigens themselves my e importnt in genetic investigtions nd popultion or fmily studies. 2. Diego (Di nd Di ). Useful s rcil mrker, Di ntigen eing lmost entirely confined to popultions of Mongolin origin, including Ntive Americns.. One hundred per cent of the white popultion types s Di(-+). 3. Colton (Co nd Co ).. Prllels the incidence of K nd k.. Approximtely 89% of the White popultion is Co(+=) nd 0.4% re Co(++). 4. Crtwright (Yt nd Yt ). Prllels the incidence of K nd k.. Approximtely 9.9% of the White popultion is Yt(+-) nd 7.9% is Yt(++). 5. Domrock (Do nd Do ). Prllels incidence of the Duffy system.. Approximte 49.5% of the White popultion is Do(++), 33.3%is Do(-+) nd 7.2% is Do(+-). L. The Sex-Linked Blood Group ntigen Xg. In 962, n ntiody ws discovered tht identified n ntigen more common mong women thn mong men.. This would e expected of n X-orne chrcteristic.. Femles inherit n X chromosome from ech prent, wheres mle inherit X only from their mother. 2. The ntigen is clled Xg in recognition of its X-orne mnner of inheritnce. 3. Anti-Xg is n uncommon ntiody tht usully rect only y the IAT, ut sline gglutinins hve een oserved. 4. This ntiody hs not een implicted in HDN or HTRs. 5. Anti-Xg my e useful for trcing the trnsmission of genetic trits ssocited with the X chromosome. M. High-Incidence RBC Antigens. High-incidence (pulic) ntigen is defined s those ntigens occurring in 92 to 99.9% or more of the generl popultion. 2. Persons mke llontiody to specific lood group ntigens due to the fct tht their own RBCs lck the offending ntigen. 3. For this reson, ntiodies directed t high- incidence ntigens re rrely encountered ecuse y definition, most of the generl popultion will hve these ntigens present on their cells. 4. When ntiodies to high frequency ntigens occur it my e exceedingly difficult to find comptile lood. IX. Other Blood Group Systems MLAB

13 . Memers of the ptient's fmily, especilly silings, re usully the most promising sources.. My hve to hve lood center contct the Rre Donor File to find potentil units. 5. Antiodies to the corresponding ntigens usully rect est y the IAT. N. Other RBC Antigens of Comprtively High Incidence. Formerly referred to s high-titer, low-vidity (HTLA). 2. Among the most frustrting prolems encountered in testing ser for unexpected ntiodies re those creted y the group of ntiodies formed to these ntigens.. Rections invrily oserved in the AHG phse of testing.. They re commonly wekly rective, vrile in rectivity nd sometimes irreproducile. 3. The term HTLA refers to the fct tht feele rections seen with undiluted serum will often persist in serum sujected to considerle dilution. 4. Rections suggests either low ffinity of the ntiody or wek cellulr expression of the ntigen, rther thn limited ntiody concentrtion. 5. Trnsfusion prctice:. These ntiodies, though of detle clinicl significnce, rect with ntigens hving firly high incidence in the popultion.. When the ntiody hs een identified, lood cn normlly e issued without dely. c. Work cn then continue to determine the ntiody specificity. O. The Sd Antigen. This ntigen is of firly high incidence nd is widely distriuted in mmmlin tissues nd ody fluids.. The ntigen is vrily expressed on the cells.. My dispper trnsiently during pregnncy. 2. Anti-Sd is most frequently detected during the AHG phse when the test is exmined microscopiclly.. Most exmples would e eqully demonstrle if the cell utton were exmined microscopiclly t IS fter resuspension.. Mixed-field gglutintion is the chrcteristic rection. 3. Urine from guine pigs nd from Sd(+) humns inhiits the rectivity of nti-sd (neutrliztion). 4. Although reported once s cusing n HTR, nti-sd is widely elieved to hve no clinicl significnce. MLAB IX. Other Blood Group Systems

14 P. Low-incidence RBC Antigens. Mny low-incidence (privte) RBC ntigen hve een recognized in ddition to growing numer tht hve een ssigned to the MN nd Rh systems. 2. These ntigens occur with frequency of in 500 or less. 3. Antiodies. Rect with so few rndom lood smples tht they virtully never cuse difficulties in selecting lood for trnsfusion.. They re only encountered y chnce in ntiody screening or comptiility testing, when screening cell or donor cell selected hppens to crry the corresponding ntigen. c. Routine ntiody screening tests rrely detect such ntiodies, the crossmtch ffords the only opportunity to detect n incomptiility, should ntigen positive lood e selected. d. The chnce of choosing donor lood positive for tht ntigen, however, is quite remote. 4. The ntiodies to these re usully sline gglutinins, ut some do occur s IgG rective t the IAT nd hve cuse HDN. Q. The Bg Antigens. Antiodies directed t certin leukocyte ntigens sometimes cuse confusing rections in serologic test with RBCs.. The Bg ntigens re expressed to vrile degrees on RBCs.. Rections of vrying strengths re oserved when serum contins nti-bg is tested with different Bg+ RBCs. c. Rectivity is most commonly oserved t IAT lthough potent nti-bg my cuse direct gglutintion of cells with strong expression of Bg ntigens. 2. Antiodies to the Bg ntigen re not cliniclly significnt in regrd to RBC trnsfusion prctice. IX. Other Blood Group Systems MLAB