High and Low incidence antibodies

• Coa: 99.5% all
• Cob: 80% European ancestry
• Co3: 100% all

Expressed on cord cells

Proteolytic enzymes

• Monosomy 7 - A rare type of dyserythropoietic anemia 
• Leukemia

May cause severe HDFN & HTR

LW(a+b-): >99%

LW(a+b+): <1%

LW(a-b+):  Very rare

LW(a-b-) : Very rare

Strongly expressed on D+ adult cells and all cord cells

Weakly expressed on D- adult cells

Rhnull are: LW (a-b-)

anti-Lwa may look like anti-D

DTT, AET, & Pronase

(D antigen is not destroyed by DTT) * How to differentiate

• Expressed stronger on D+ than D- cell
• Even Stronger on cord cells
• No expressed on Rhnull or LWnull phenotypes

• IAT phase
• Not clinically significant (No HDFN or HTR

• Sometimes associated with:
• pregnancy or hematologic malignancy

• Found on the fourht component of complement 4
• Formerly known as HTLA

• They are NOT intrinsic to the red cell 
• Are ABSORBED onto the red cell from plasma

• IgG
• IAT

• **Neutralization: Antigen positive serum or plasma - Use for serological problem solving
• OR
• Adsorption with red cells coated with C4

NO - HTR or HDFN

Ficin/papain/trypsin: Sensitive

DTT, Chloroquine (RT): Resisitant

• Ge2
• Ge3,
• GEPL
• GEAT
• GETI

• Wb
• Lsa
• Ana
• Dha
• GEIS

Ge2 & 4 Destroyed by: Trypsin & Papain

• Ge3 destroyed by: Trypsin
• Ge3 resistant to: Papain

Papain distinguishes 3 form 2 & 4

• IgG - Mostly
• IAT
• No - HTR

Ge3 may cause HDN (2-4wks post delivery)

Located on the complement regulatory glycoprotein, decay accelerating factero (DAF or CD55)

Tca & WEb

Tcb, Tcc, & WEa

• Destroyed by: a-chymotrypsin
• Only Slightly reduced: AET & DTT
• Resistant: papain, ficin, trypsin

• Not clinically significant
• IgG
• IAT

*** Are inhibited by serum or concentrated urine from antigen positive individuals and are removed from serum by platelet concentrates.

anti-IFC

*****KNOW: Cromer located on red cell membrane complement regulatory protein called Decay Accelerating Factor (DAF) and that the Null phenotype Inab, lacks DAF and therefore lacks all CROM antigens and can produce anti-IFC, which can be clinically significant.******

• IgG
• IAT
• Neutralization: Soluble CR1

Are NOT clnicaly significant & can be ignored when selecting blood. *** Give least incompatible due to the likelihood of having a positive XM.

Indicates very low levels of red cell CR1 and very weak expression of Knops antigens

Resistant to: Papain & ficin

Destroyed by trypsin and a-chymotrypsin

Weakened or possibly destroyed by: AET & DTT

CR1 appears to be involved in resetting of red cells that is associated with severe P. falciparum malaria

Parasites

• Ina (Arg46) = Low
• Inb (Pro46) = High
• Wj = High

Reduced expression in the presence of In(Lu) phenotype

Often direct agglutinate, but IAT usually enhances.

• Not considered clinically significant
•   **** However, there is one report of Inb causing HTR

Causes severe HTR

In(Lu) red cells should be selected for transfusion.

High prevalence

Oka - Resistant to: AET & DTT

Reactive by IAT

Possibly clinically significant

Located on CD44, they glycosaminoglycan hyaluronan, a component of the extracellular matrix

Only 3 Jews identified as RAPH null phenotype

React in IAT - not clinically significant

Resistant to: Papain

Destroyed by: Trypsin, a-chymotrypsin, pronase, AET, & DTT

• Typically produced by thos who acquire CD108
• In elderly, sometimes associated with weak DAT's
• Reactive in IAT
• **Not considered clinically significant, however 1 case has resulted in acute HTR

• Destroyed by: proteolytic enzymes (AET & DTT)
• Not detected on cord cells

• High prevalence
• Located on aquaporin 3, a member of the aquaporin superfamily of water and glycerol channels.
• Enhances permeability of RBC membrane by glycerol and water

IAT

Resistant to AET & DTT

• Ola is rare
• Associated with Rhmod phenotype

RHAG4 is low prevalence - one case associated wit HDFN

Duclos & DSLK high prevalence

New blood group

Found on two donors from different families with the Apae phenotype

Naturally occurring Ab.

High Prevalence

Jra associated with drug resistance in cancer and Xenobiotics

Might be important in porphyrin hemostasis

Seen mostly in Japanese ancestry

IAT - Can cause HTR and HDFN

Resistant to AET & DTT

High Prevalence

IAT

Yes to HTR & HDFN

High Prev

Antigen expression is very weak on crod cells and varies from one person to antoher

• Mixture of IgG & IgM
• Readily activates complement 
• HTR yes
• HDFN (though rare)

• Agglutination of Sda+ cells may produce a "mixed-field" appearance
• When viewed microscopically, the agglutinates are retractile
• Inhibited by urine for Sda+ individuals and guinea pig urine
• Carried on Tam Horsfall Glycoprotein

• Class I
• Bga represents HLA-B7
• Bgb =  HLA-B17 (57 or 58)
• Bgc = HLA-A28 (68 OR 69)

Many do not express Bg antigens despite having the corresponding HLA antigen on their lymphocytes.

Nuisance antibodes (sometimes contaminants in reagens)

Destroyed by papain, ficin, pronase, trypsin, a-chymotrypsin, AET, & DTT

Can be stripped form red cells with chloroquine (method 2-20) or EDTA/glycine-HCL (method 2-21)

Seen in mono, leukemias, polycythemia, & hemotlytic anemias

• Ge2 & 3
• Cra
• Vel - Weak on cord
• Ata - Negative only in blacks
• Oka
• AnWj - Not on cord