DUFFY, KIDD, LU

First human gene to be assigned to a specific chromosome

Duffy

Duffy antigen is Identified on fetal RBCs as early as

6 weeks gestational age and are well developed at birth

Fy (a-b-) RBCs resist infection by

Plasmodium knowlesi and also Plasmodium vivax

Resistant to malaria

Fy (a-b-) RBCs

Duffy Ag are found in

platelets, lymphocytes, monocytes, granulocytes

brain, colon, endothelium, lungs, spleen, thyroid, thymus and kidney cells

● Antithetical antigens (produced by a single gene but expressed on a different allele)

● Sensitive to ficin or papain treatment

𝐹𝑦𝑎 and 𝐹𝑦𝑏

Fy(a-b-)

Fy:-6

Fy:-3

● Common in Whites

● Altered expression in Rhnull phenotype

● Possible antigen interaction between Duffy and Rh proteins

Fy5

● Sensitive to ficin or papain treatment

Fy6

Fy6 Antigen has been defined by

murine monoclonal antibodies

The Duffy glycoprotein is a member of the superfamily of chemokine

receptors known as the

Duffy antigen receptor for chemokines (DARC).

Duffy glycoprotein binds a variety of

proinflammatory cytokines

Chinese -

Fy(a+b-)

Whites -

Fy(a+b+)

Black -

Fy(a-b-)

Discovered Kidd BGs

In 1951, Allen and colleagues

Jka has been detected on fetal RBCs

as early as 11 weeks

Jkb has been detected at

7 weeks.

can also be derived by the action of a dominant suppressor gene

Jk (a-b-) phenotype

In (Jk) for

“Inhibitor”.

If ever you have the Jk (a-b-), you have the suppressor gene In

K,

Jk (a-b-) is a common allele in

Polynesians, Filipinos and Chinese

The genotype which will lead to a result of Jk (a-b-)

Jk-Jk

has been associated with severe immediate and delayed HTRs and with mild

HDFN.

Anti-Jk3

Anti-Jka and Anti- Jkb Agglutination reactions are best observed by

the

IAT

Anti-Jka and Anti- Jkb Antibody reactivity can also be enhanced by using:

● LISS or PEG

Found in the serum of a patient with lupus erythematous

Anti-Lua

The first Ab that is discovered under the Lutheran blood group system are the

anti-Lua

How many ag are part of the Lutheran system

20 antigens

LU AGs Detected on fetal RBCs as early as

10-12 weeks of gestation

Poorly developed at birth

may result in adsorption of maternal antibodies to lutheran antigens

○ Decreasing the likelihood of HDFN (Hemolytic Disease of Fetus and

Newborn)

Presence of lutheran glycoprotein on placental tissue

Produced by allelic codominant genes, just like the ABO blood group.

Lua and Lub antigen:

IgM naturally occurring saline agglutinins. It will react better at room temperature than 37°C.

Anti-Lua

Anti-Lua Can show a characteristic of what agglutination

mixed field pattern of agglutination

It has no clinical significance in transfusion.

Mild cases of HDFN have been reported.

Anti-Lua

Mostly IgG, but IgM and IgA antibodies have also been noted.

- Most examples are IgG and reactive at 37°C at antiglobulin phase.

Anti-Lub

Made in response to pregnancy or transfusion.

- Implicated with shortened survival of transfused cells and post transfusion jaundice.

- Severe or acute hemolysis has not been reported.

Anti-Lub

Rarely occurs and may manifest itself in any of the following three unique genetic mechanisms

𝑳𝒖𝒏𝒖𝒍𝒍 phenotype or Lu(a-b-)

homozygosity for a rare recessive amorph, Lu, at the LU locus.

Recessive: only true 𝑳𝒖𝒏𝒖𝒍𝒍 phenotype;

heterozygosity for a rare dominant inhibitor gene, In(Lu), that is not located at the LU locus.

Dominant inhibitor or In (Lu) phenotype:

inherited in a recessive manner

X-linked suppressor gene:

Rare antibody that reacts with all RBCs

Anti-Lu3

Anti-Lu3 reacts with all RBCs except

Lu(a-b-) RBC

● Usually antiglobulin reactive.

● Made only by individuals with the recessive type of Lu(a-b-).

Anti-Lu3

Clinically Significant BGs

ABO, Rh, Kell, Kidd,

Duffy, S, s, and U, Lutheran (𝐿𝑢𝑏)

Usually Clinically Insignificant BGs

I, Lewis, M, N,

P1, Lutheran (𝐿𝑢𝑎)