BB CH 8
Content
BB CH 8 – BLOOD GROUP TERMINOLOGIES AND OTHER BLOOD GROUP
Code
徐智慧/ Ab Anti-M Cold IgM/ IgG Anti-N Cold IgM/ IgG Anti-S anti-s IgG Anti-U IgG Antibody Anti-N ▪ doesn’t bind complement ▪ doesn’t react with enzyme treated RBC ▪ often shows dosage ▪ react better with M-N+ than M+N+ ▪ seen in renal px ▪ SF: doesn’t react at 37 HDN Anti-M (IgG) Anti-N Rare Anti-S YES Anti-U YES HTR Anti-M Rare Anti-N No Anti-S YES Anti-U YES
002
Name MNS
Antigen M and N ▪ Codominant alleles (can be used in paternity testing) ▪ found on glycophorin A (GPA), Sialoglycoprotein (SGP) ▪ antithetical ▪ differ in amino acid resides at position 1 and 5 M N Serine 1 Leucine 1 Glycine 5 Glutamic acid 5
S and s ▪ located on GPB (smaller than GPA) S s Methionine at 29 Threonine at 29 ▪ less easily degraded by enzymes ▪ enzyme sensitive sites are less accesible ▪ Destroyed by: ficin, papain, bromelin, pronase, chymotrypsin
▪ Altered by Formaldehyde to be foreign antigen ▪ Well developed at birth ▪ 106 copies of GPA/RBC ▪ located on outer end of GPA, easily destroyed by routine blood bank enzyme ficin, papain, bromelin, trypsin, pronase ▪ destroyed by ZZAP, DDT + papain/ficin, AET, αchymotrypsin, chloroquine, glycine acid EDTA ▪ Treat RBC with neuraminidase, cleaves sialic acid, abolish reactivity with some antibody 003 P1PK
U antigen ▪ located on GPB33, 39 (high prevalence) ▪ resistant to enzyme treatment
Anti-M ▪ naturally occuring saline ▪ reacts below 37C ▪ doesn’t bind complement ▪ doesn’t react with enzyme treated RBC ▪ children > adults ▪ common in px with bacterial infection ▪ may require serum acidification ▪ often shows dosage ▪ SF : 37C ▪ reactivity enhancer: ↑ serum:cell ration ↓ incubation time, temp Add potentiating medium Anti – P1 ▪ weak ▪ cold reactive 4C ▪ saline agglutinin ▪ bind complement
Anti-S & anti-s ▪ show dosage ▪ don’t react with enzyme treated RBC ▪ more significant than M/N ▪ bind complement ▪ SF: 37C
Anti-U (S-s-U) ▪ Lacks S and s antigen ▪ Blacks ▪ IgG ▪ heterogenous ▪ doesn’t react with M+N-S-s-
Resistant to enzyme treatement P Platelet Ept.cell Fibrobl ast P, P1, P Lymph ocyte RBC Granul ocyte Manoc yte
K
P, P Plasma Hydatid cyst fluid
K
P = Chromosome 3 P1, PK = Chromosome 22 005 LUTHERAN ▪ Lua and Lub ▪ produced by allelic codominant genes ▪ mostly Lu(b+) ▪ 18 antigens coded by Lu gene at chromosome 19 ▪ linked to Se gene ▪ High incidence: Lu4, Lu5, Lu7, Lu12, Lu13, Lu20 (absent from Lu a-b-) Located on glycoprotein 3 POSSIBLE CAUSES OF Lu(a-b-) phenotype Dominant In (Lu) ▪ RBC may have trace amt of Lu antigen (adsorption, elution) ▪ Inheritance prevents expression of all lutheran antigens ▪ may affect RBC shape and metabolism (poikilocytosis, acanthocytosis) Lu(w) phenotype Lu(a-b+w) and Lu(a+wb+w) ▪ weak expression of Lu antigen ▪ due to weaker In(Lu) gene 006 KELL K and k antigen ▪ K = 2nd most immunogenic ▪ low prevalence Kpa, Kpb, Kpc ▪ a,c =Low prevalence ▪ b = high prevalence ▪ a = suppression of k & Jsb Jsa, Jsb ▪ a = low prevalence ▪ b = high prevalence
Anti-P1 IgM AntiPP1PK IgM/ IgG Allo anti-P IgM/ IgG Auto anti-P IgG AntiLua IgM AntiLub IgG
Anti-PP1PK ▪ spontaneous abortion in early pregnancy ▪ bind complement ▪ react with wide thermal range
Alloanti-P ▪ naturally occuring ▪ habitual early abortion
Autoanti-P ▪ cold reactive IgG ▪ ~PCH (Paroxysmal Cold Hemoglobinuria) ▪ biphasic hemolysin ▪ demonstrable only by Donath Landsteiner test
Anti-P1 NO AntiK PP1P YES
Anti-P1 (IgG) AntiK PP1P YES
Anti-Lua ▪ naturally occurring ▪ IAT: few reacts at 37C ▪ may exist as IgG/IgA
Anti-Lub ▪ may exist as IgM/IgA ▪ reacts with all cells ▪ doesn’t react with autocontrol ▪ weak reaction with Lu(a+b+) ▪ jaundice, shortened rbc survival ▪ CF
Anti-Lu3 ▪ made by recessive Lu(a-b-) ▪ rare, reacts with all RBC ▪ antiglobulin reactive
AntiLua NO AntiLub mild
AntiLua
delayed
AntiLub NO
Recessive Lulu ▪ inheritance of 2 rare silence alleles ▪ makes anti-Luab or anti-Lu3
Recessive X-linked inhibitor ▪ Seen in males (carrier) ▪ weak P1 and I but i was well expressed
Anti-K IgG
007
LEWIS
▪ Intrinsic to Type I Glycosphingolipids
Lea = present in secretion only
IgM
Anti-K ▪ Induced by pregnancy & transfusion ▪ IgM are rare ▪ Most reliable detection: IAT ▪ bind complement ▪ naturally occuring
Anti-Kpa, anti-Jsa ▪ rare ▪ result from transfusion/ pregnancy
Anti-k, anti-Kpb, anti-Jsb ▪ rare
Anti-K YES AntiKpa, Jsa YES NO
Anti-K YES
RARE
▪ Passively adsorbed to Plasma membrane ▪ Lewis FUT 3 = FUT2 se, FUT1 H ▪ Chromosome 19 ▪ Le (a-b-) = Africans ▪ Le (a+b+) = asians ▪ Diminished in Mom’s RBC during pregnancy ▪ Not in cord RBC ▪ Present in Lymphocyte, Platelet, Tissue ▪ Present in saliva (glycoprotein) ▪ Resistant to enzymes
Le = present in RBC and secretion (Le Se) (lele, sese) Le(a-b-) = newborn Le(a-b-) = forever Le(a+b-) = 10 days Le(a+b+) Le(a-b+) = 6 years (Le sese) Le(a-b-) = birth Le(a+b-) = 10 days- life
b
▪ agglutinate saline suspended RBC ▪ Can bind complement ▪ IgM ▪ don’t cross placenta ▪ not well developed on fetal RBC ▪ Neutralized by lewis substance in plasma/saliva Anti-Lea ▪ 37C, RT ▪ IAT ▪ 80% Secretors ▪ in vitro hemolysis of incompatible RBC
Anti-Leb ▪ Anti-LeBh (Leb, H) Bl b ▪ Anti-Le (Le , H)
008
DUFFY
Fy , Fy 6 weeks gestational age= identified Birth = well developed Located on: body tissues, brain, colon, endothelium, lung, spleen, thyroid, thymus, kidney cells ▪ Destroyed by common proteolytic enzyme and ZZAP ▪ Fy (a-b-) RBC resist infection by malaria organism Plasmodium vivax ▪ well developed on RBC of neonates ▪ Jka = detected on fetal RBC = 11 weeks ▪ Jkb = detected on fetal RBC = 7 weeks ▪ Not very immunogenic
a
b
IgG
▪ Anti-Fy is more common than Anti-Fy ▪ rarely bind complement ▪ enhanced in LISS ▪ Don’t react with enzyme treated cells ▪ shows dosage ▪ Fy = blacks, silent allele (single dose), white = double dose ▪ Anti-Jka, anti-Jkb ▪ show dosage ▪ often weak ▪ may bind complement ▪ response during pregnancy or transfusion ▪ enhanced with LISS, PEG, enzymes
b
a
YES
YES
009
KIDD
IgG
RARE
YES
019
KX
027
I and i
Mcleod phenotype ▪ affects males only ▪ rare ▪ abnormal RBC morphology, compensated hemolysis anemia, neurological and muscular abnormalities ▪ X-Linked chronic granulomatous disease I antigen i antigen IT ▪ adult RBC ▪ major in infant RBC ▪ Transition between I ▪ Increased sensitivity when ABH antigen are and i removed Found on: leukocyte membranes, RBC, platelets, serum & plasma (adults), saliva (newborns), human milk, amniotic fluid, ovarian cyst, urine. ▪ not antithetical ▪ have reciprocal relationship
IgM
Anti-I ▪ Enhanced by enzymes ▪ Allo antibody, interfere with Ab screening ▪ Auto antibody, causes Cold AIHA, Cold agglutinin syndrom,e after mycoplasma pneumoniae ▪ reacts with all adult cells (except rare i adult) ▪ benign, weak, naturally occuring ▪ detectable at 4C only
Anti-i ▪ Auto antibody – IM, reticuloses, myeloid leukemia, Alcoholic cirrhosis
Anti-IT ▪ Cold agglutinin : in melanesians, Yanomama Indians in venezuela
Anti-i (IgG)
徐智慧/
Code
徐智慧/ Ab Anti-M Cold IgM/ IgG Anti-N Cold IgM/ IgG Anti-S anti-s IgG Anti-U IgG Antibody Anti-N ▪ doesn’t bind complement ▪ doesn’t react with enzyme treated RBC ▪ often shows dosage ▪ react better with M-N+ than M+N+ ▪ seen in renal px ▪ SF: doesn’t react at 37 HDN Anti-M (IgG) Anti-N Rare Anti-S YES Anti-U YES HTR Anti-M Rare Anti-N No Anti-S YES Anti-U YES
002
Name MNS
Antigen M and N ▪ Codominant alleles (can be used in paternity testing) ▪ found on glycophorin A (GPA), Sialoglycoprotein (SGP) ▪ antithetical ▪ differ in amino acid resides at position 1 and 5 M N Serine 1 Leucine 1 Glycine 5 Glutamic acid 5
S and s ▪ located on GPB (smaller than GPA) S s Methionine at 29 Threonine at 29 ▪ less easily degraded by enzymes ▪ enzyme sensitive sites are less accesible ▪ Destroyed by: ficin, papain, bromelin, pronase, chymotrypsin
▪ Altered by Formaldehyde to be foreign antigen ▪ Well developed at birth ▪ 106 copies of GPA/RBC ▪ located on outer end of GPA, easily destroyed by routine blood bank enzyme ficin, papain, bromelin, trypsin, pronase ▪ destroyed by ZZAP, DDT + papain/ficin, AET, αchymotrypsin, chloroquine, glycine acid EDTA ▪ Treat RBC with neuraminidase, cleaves sialic acid, abolish reactivity with some antibody 003 P1PK
U antigen ▪ located on GPB33, 39 (high prevalence) ▪ resistant to enzyme treatment
Anti-M ▪ naturally occuring saline ▪ reacts below 37C ▪ doesn’t bind complement ▪ doesn’t react with enzyme treated RBC ▪ children > adults ▪ common in px with bacterial infection ▪ may require serum acidification ▪ often shows dosage ▪ SF : 37C ▪ reactivity enhancer: ↑ serum:cell ration ↓ incubation time, temp Add potentiating medium Anti – P1 ▪ weak ▪ cold reactive 4C ▪ saline agglutinin ▪ bind complement
Anti-S & anti-s ▪ show dosage ▪ don’t react with enzyme treated RBC ▪ more significant than M/N ▪ bind complement ▪ SF: 37C
Anti-U (S-s-U) ▪ Lacks S and s antigen ▪ Blacks ▪ IgG ▪ heterogenous ▪ doesn’t react with M+N-S-s-
Resistant to enzyme treatement P Platelet Ept.cell Fibrobl ast P, P1, P Lymph ocyte RBC Granul ocyte Manoc yte
K
P, P Plasma Hydatid cyst fluid
K
P = Chromosome 3 P1, PK = Chromosome 22 005 LUTHERAN ▪ Lua and Lub ▪ produced by allelic codominant genes ▪ mostly Lu(b+) ▪ 18 antigens coded by Lu gene at chromosome 19 ▪ linked to Se gene ▪ High incidence: Lu4, Lu5, Lu7, Lu12, Lu13, Lu20 (absent from Lu a-b-) Located on glycoprotein 3 POSSIBLE CAUSES OF Lu(a-b-) phenotype Dominant In (Lu) ▪ RBC may have trace amt of Lu antigen (adsorption, elution) ▪ Inheritance prevents expression of all lutheran antigens ▪ may affect RBC shape and metabolism (poikilocytosis, acanthocytosis) Lu(w) phenotype Lu(a-b+w) and Lu(a+wb+w) ▪ weak expression of Lu antigen ▪ due to weaker In(Lu) gene 006 KELL K and k antigen ▪ K = 2nd most immunogenic ▪ low prevalence Kpa, Kpb, Kpc ▪ a,c =Low prevalence ▪ b = high prevalence ▪ a = suppression of k & Jsb Jsa, Jsb ▪ a = low prevalence ▪ b = high prevalence
Anti-P1 IgM AntiPP1PK IgM/ IgG Allo anti-P IgM/ IgG Auto anti-P IgG AntiLua IgM AntiLub IgG
Anti-PP1PK ▪ spontaneous abortion in early pregnancy ▪ bind complement ▪ react with wide thermal range
Alloanti-P ▪ naturally occuring ▪ habitual early abortion
Autoanti-P ▪ cold reactive IgG ▪ ~PCH (Paroxysmal Cold Hemoglobinuria) ▪ biphasic hemolysin ▪ demonstrable only by Donath Landsteiner test
Anti-P1 NO AntiK PP1P YES
Anti-P1 (IgG) AntiK PP1P YES
Anti-Lua ▪ naturally occurring ▪ IAT: few reacts at 37C ▪ may exist as IgG/IgA
Anti-Lub ▪ may exist as IgM/IgA ▪ reacts with all cells ▪ doesn’t react with autocontrol ▪ weak reaction with Lu(a+b+) ▪ jaundice, shortened rbc survival ▪ CF
Anti-Lu3 ▪ made by recessive Lu(a-b-) ▪ rare, reacts with all RBC ▪ antiglobulin reactive
AntiLua NO AntiLub mild
AntiLua
delayed
AntiLub NO
Recessive Lulu ▪ inheritance of 2 rare silence alleles ▪ makes anti-Luab or anti-Lu3
Recessive X-linked inhibitor ▪ Seen in males (carrier) ▪ weak P1 and I but i was well expressed
Anti-K IgG
007
LEWIS
▪ Intrinsic to Type I Glycosphingolipids
Lea = present in secretion only
IgM
Anti-K ▪ Induced by pregnancy & transfusion ▪ IgM are rare ▪ Most reliable detection: IAT ▪ bind complement ▪ naturally occuring
Anti-Kpa, anti-Jsa ▪ rare ▪ result from transfusion/ pregnancy
Anti-k, anti-Kpb, anti-Jsb ▪ rare
Anti-K YES AntiKpa, Jsa YES NO
Anti-K YES
RARE
▪ Passively adsorbed to Plasma membrane ▪ Lewis FUT 3 = FUT2 se, FUT1 H ▪ Chromosome 19 ▪ Le (a-b-) = Africans ▪ Le (a+b+) = asians ▪ Diminished in Mom’s RBC during pregnancy ▪ Not in cord RBC ▪ Present in Lymphocyte, Platelet, Tissue ▪ Present in saliva (glycoprotein) ▪ Resistant to enzymes
Le = present in RBC and secretion (Le Se) (lele, sese) Le(a-b-) = newborn Le(a-b-) = forever Le(a+b-) = 10 days Le(a+b+) Le(a-b+) = 6 years (Le sese) Le(a-b-) = birth Le(a+b-) = 10 days- life
b
▪ agglutinate saline suspended RBC ▪ Can bind complement ▪ IgM ▪ don’t cross placenta ▪ not well developed on fetal RBC ▪ Neutralized by lewis substance in plasma/saliva Anti-Lea ▪ 37C, RT ▪ IAT ▪ 80% Secretors ▪ in vitro hemolysis of incompatible RBC
Anti-Leb ▪ Anti-LeBh (Leb, H) Bl b ▪ Anti-Le (Le , H)
008
DUFFY
Fy , Fy 6 weeks gestational age= identified Birth = well developed Located on: body tissues, brain, colon, endothelium, lung, spleen, thyroid, thymus, kidney cells ▪ Destroyed by common proteolytic enzyme and ZZAP ▪ Fy (a-b-) RBC resist infection by malaria organism Plasmodium vivax ▪ well developed on RBC of neonates ▪ Jka = detected on fetal RBC = 11 weeks ▪ Jkb = detected on fetal RBC = 7 weeks ▪ Not very immunogenic
a
b
IgG
▪ Anti-Fy is more common than Anti-Fy ▪ rarely bind complement ▪ enhanced in LISS ▪ Don’t react with enzyme treated cells ▪ shows dosage ▪ Fy = blacks, silent allele (single dose), white = double dose ▪ Anti-Jka, anti-Jkb ▪ show dosage ▪ often weak ▪ may bind complement ▪ response during pregnancy or transfusion ▪ enhanced with LISS, PEG, enzymes
b
a
YES
YES
009
KIDD
IgG
RARE
YES
019
KX
027
I and i
Mcleod phenotype ▪ affects males only ▪ rare ▪ abnormal RBC morphology, compensated hemolysis anemia, neurological and muscular abnormalities ▪ X-Linked chronic granulomatous disease I antigen i antigen IT ▪ adult RBC ▪ major in infant RBC ▪ Transition between I ▪ Increased sensitivity when ABH antigen are and i removed Found on: leukocyte membranes, RBC, platelets, serum & plasma (adults), saliva (newborns), human milk, amniotic fluid, ovarian cyst, urine. ▪ not antithetical ▪ have reciprocal relationship
IgM
Anti-I ▪ Enhanced by enzymes ▪ Allo antibody, interfere with Ab screening ▪ Auto antibody, causes Cold AIHA, Cold agglutinin syndrom,e after mycoplasma pneumoniae ▪ reacts with all adult cells (except rare i adult) ▪ benign, weak, naturally occuring ▪ detectable at 4C only
Anti-i ▪ Auto antibody – IM, reticuloses, myeloid leukemia, Alcoholic cirrhosis
Anti-IT ▪ Cold agglutinin : in melanesians, Yanomama Indians in venezuela
Anti-i (IgG)
徐智慧/
