Other Blood Group Systems Flashcards
GPI linked glycoprotein on acetylcholinesterase
Yt
Yt antigens
Yta- high prevalence in all pop.
Ytb- 8% except in israeli’s where it can be up to 26%
No known null phenotype
Yta antigen w/ enzyme or DTT treatment
Destroyed
Yt antibodies
Usually IgG
No HDFN
anti-yta may cause HTR
Yta with trypsin and a-chymotrypsin
Trypsin-not effected
A-chymptrypsin- destroyed
XG blood group antigens
Xga and CD99
XG gene locations
XG : Xp22.32 tip of the short arm- not inactivated by lyonization
CD99 gene is on both X and Y chromosome
Xga prevalence
66% males
89% females
Anti-Xga
Usually IgG reactivity at IAT
Not considered clinically significant
Xga with ficin
Sensitive
Xga with DTT/AET
Resistant
Colton antigens
Co^a, Co^b, Co3, Co4
High prevalence Colton antigens
Co^a, Co3, Co4
Co^b prevalence
10%
Colton antigen location
Aquaporin-1 (red cell water transporter)
Colton gene location
Chromosome 7p14
Colton antibodies
usually IgG
Implicated in HDFN and HTRs
Colton antigen with proteolytic enzymes
Resistant
Anti-Co3
Made by rare Co(a-b-) phenotypes caused by various inactivating mutations
Co4
Required for Co^a expression
Gerbrich high prevalence antigens (6)
Ge2, Ge3, Ge4, GEPL, GEAT, GETI
Gerbrich low prevalence antigens (5)
Wb, Ls^a, An^a, Dh^a, GEIS
Gerbrich antigen locations
GPC and GPD- part of a junctional complex of membrane proteins that interact with protein 4.1 and p55 that help link membrane and it’s skeleton for membrane stability
Gerbrich gene location
Chromosome 2q14-21
GPC receptor for what parasite/virus
Plasmodium falciparum
Influenza A and B
Gerbrich null
Ge:-2,-3,-4
Both GPC and GPD absent
Cells are eliptocytes
Yus phenotype
Ge:-2,3,4
Make anti-Ge2
No depression of Kell/Vel antigens
Lack GPD with altered GPC
Gerbich phenotype
Ge:-2,-3,4
Make anti-Ge2 and/or -Ge3
Weakened Kell/Vel expression
Lack GPD with altered GPC
Leach phenotype
Ge:-2,-3,-4
Make antibodies to all
Decreased Kell/Vel expression
Lack GPC and GPD
Elliptocytes
Gerbrich antigens with treatment
Trypsin: destroyed
Papain: destroys Ge2,4; Ge3 resistant
Distinguish anti-Ge2 from anti-Ge3 in absence of rare cells
Use papain treated cells
Gerbrich antibodies
Usually IgG but may be IgM
Usually not clinically significant but anti-Ge3 has caused mild HTR/HDFN
Cromer antigen location
Decay-accelerating factor (CD55)- a complement regulatory glycoprotein
Cromer low incidence antigens
Tc^b, Tc^c, and WES^b
Other 15 are high frequency
Cromer null
Inab phenotype
Make anti-IFC
Cromer antigen with cell treatment
Destroyed by a-chymotrypsin
Resistant to papain, ficin, and trypsin
Weakened by AET/DTT
Cromer antigen is a receptor for what parasite
Plasmodium falciparum
Cromer antibodies
Usually IgG
Not usually considered to be clinically significant
Inhibited by serum or concentrated urine of antigen positive individuals
Dombrock gene location
Chromosome 12p13
Do a/b frequency
Whites
Do(a+b-): 18%
Do(a+b+): 49%
Do(a-b+): 33%
Do a/b prevalence
African American
Do(a+b-): 11%
Do(a+b+): 44%
Do(a-b+): 45%
Dombrock null phenotype
Gya-
Result of various inactivating mutations
Make anti-Gya
Hy- and Jo(a-)
Uncommon phenotypes
Negative or weak expression of dombrock antigens
Dombrock antigens on treated cells
Resistant to papain and ficin
Sensitive to trypsin, a-chymotrypskn, pronase
Sensitive to DTT/AET
Dombrock antibodies
Typically IgG
Usually weakly reactive
Have been implicated in HTRs but no HDFN
Indian antigen location
CD44- cell surface receptor for glycosaminoglycan hyaluranan
Indian antigen/ prevalence
In^a: low
In^b: high
INFA, INJA, INRA: high
Indian antigens with RBC treatment
Sensitive: papain, ficin, trypsin, a-chymotrypsin. As well as DTT/AET
Indian antigen weak expression on
Cord cells
In(Lu)
Indian antibodies
Not generally clinically significant
Anti-Inb has caused HTR
Vel blood group
1 antigen: Vel- high incidence
Vel antigen expression
Weak on cord cells
Variable expression among individuals
Vel effect on treated RBCs
Enhanced by enzymes
Variable effect with DTT/AET
Anti-Vel
Often a mix of IgM and IgG
Readily activated complement
Cause of severe HTRs though HDFN is rare
Diego antigen location
Band 3, red cell anion exchanger
Diego gene location
Chromosome 17q21.31
Di^a prevalence
Rare in European and African
5% Asian
Up to 50% in n. and s. American indigenous people
Di^b prevalence
High prevalence in all populations
Diego Dia and Dib antibodies
Usually IgG reactivity at IAT
May cause HDFN but no known HTRs
Wra/Wrb
Wra: low
Wrb: high
Expression dependent on GPA presence
Anti-Wra
Usually IgG
Relatively common
Responsible for severe HDFN and HTRs
Diego antigen on treated RBCs
Resistant to proteolytic enzymes ficin, trypsin, and papain
Antigens on 3rd extracellular loop sensitive to a-chymotrypsin
Chido /Rogers antigen location
On fragment of C4d (complement component) that attaches to RBCs from plasma
NOT PRODUCED BY RBCS
Chido/Rogers antigen on treated RBCs
Destroyed by proteolytic enzymes (papain, ficin)
Chido/Rogers antibodies
Generally IgG detected at IAT
No known HDFN/HTRs but may cause anaphylactic reactions
Inhibited by plasma of Ch/Rg+ individuals