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In the ISBT classification, RBC antigens are assigned a | Six-digit identification number: |
The Le gene codes for | L-fucosyltransferase, |
The Le gene is needed for the expression of Lea substance, and Le and Se genes are needed to form | Leb substance. |
Lewis antibodies are generally (Blank) and made by (blank) | IgM (naturally occurring) made by Le(a–b–) individuals. |
Frequently encountered in pregnant women. | Lewis antibodies |
Not considered significant for transfusion medicine. | Lewis antibodies |
Is produced by the rare p individuals early in life without RBC sensitization and reacts with all | Anti-PP1Pk |
The autoanti-P of PCH usually does not react by routine tests but is demonstrable as | Biphasic hemolysin only in the Donath-Landsteiner test. |
Relationship of I and i antigens | Antithetical, reciprocal relationship |
At birth, infant RBCs are rich in i; I is almost undetectable; over the next | 18 months , the infant’s RBCs will convert from i to I antigen. |
Typically a strong cold autoagglutinin that demonstrates high-titer reactivity at 4°C and reacts over a wide thermal range (up to 30°–32°C). | Pathogenic anti-I |
Are cold-reactive saline agglutinins that do not bind complement or react with enzyme treated cells;may demonstrate dosage effect | Anti-M and Anti-N |
Are IgG antibodies, reactive at 37°C and the antiglobulin phase. They may bind complement and have been associated with HDFN and HTRs. | Anti-S and anti-s |
In MNS blood system, it is usually an IgG antibody and has been associated with HTRs and HDFN. | Anti-U |
Excluding ABO, the K antigen is rated second only to | D antigen in immunogenicity. |
Affecting only males, is described as a rare phenotype with decreased Kell system antigen expression. | Mcleod phenotype |
Also have the X-linked chronic granulomatous disease. | McLeod phenotype |
Are usually IgG antibodies and react optimally at the antiglobulin phase of testing; both antibodies have been implicated in delayed HTRs and HDFN. | Anti-Fya and anti-Fyb |
May demonstrate dosage, are often weak, and found in combination with other antibodies; both are typically IgG and reactive in the antiglobulin test. | Anti-Jka and anti-Jkb |
May bind complement and are made in response to foreign RBC exposure during pregnancy or transfusion. | Kidd antibodies |
Antibodies are a common cause of delayed HTRs. | Kidd system antibodies |
Phenotype is rare and may result from three different genetic backgrounds; only individuals with the recessive type Lu(a–b–) can make anti-Lu3. | The Lu(a–b–) phenotype |
Are located on a major RBC protein, band 3, also known as the RBC anion exchanger (AE1). | The Diego system antigens |
Are generally considered to be clinically significant; all have caused severe HTRs and HDFN | Anti-Dia, anti-Dib, and anti-Wra |
Are rare and little is known about their clinical significance, has been observed in the Marshall Islands and New Guinea. | Scianna system antigens |
Are located on the complement fragments C4B and C4A, respectively, that are adsorbed onto RBCs from plasma. | Chido/Rodgers system |
React weakly, often to moderate or high-titer endpoints in the antiglobulin test and may be tentatively identified by plasma inhibition methods. | Anti-Ch and anti-Rg |
Are very rare outside of Papua, New Guinea. | Gerbich-negative phenotypes |
Are carried on the decay accelerating factor and are distributed in body fluids and on RBCs, WBCs, platelets, and placental tissue. | Cromer antigens |
1. The following phenotypes are written incorrectly except for: a. Jka+ b. Jka+ c. Jka(+) d. Jk(a+) | D |
Lewis antibodies are increased in | Pregnancy |
Characteristics of Anti-i except: | IgM in nature |