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Published on: January 2, 2013
Kidd blood group system: a review
1MS, MT(ASCP)SBB, American Red Cross-Southeastern Michigan Region, Manager, Immunohematology Reference Laboratory, PO Box 33351, 100 Mack Ave., Detroit, MI 48232-5351.
Insights
The Kidd blood group system, crucial in blood transfusion, involves the JK glycoprotein, a urea transporter. Genetic variations lead to diverse antigen expressions and null phenotypes across populations.
Area of Science:
- Hematology
- Genetics
- Immunology
Background:
- The Kidd blood group system is clinically significant in red blood cell (RBC) serology.
- The JK glycoprotein, identified as the urea transporter UT-B, is encoded by SCL14A1.
- Its role in RBC and kidney urea transport is well-established.
Purpose of the Study:
- To review the historical context of Kidd antigens and antibodies.
- To catalog the genetic variations within the JK gene.
- To highlight the expanding understanding of the Kidd blood group system.
Main Methods:
- Literature review of historical data on Kidd antigens and antibodies.
- Analysis of genetic polymorphisms within the JK gene (SCL14A1).
- Examination of reported null and variant phenotypes across diverse populations.
Main Results:
- The JK system includes 23 alleles causing null expression and 7 causing weak/partial antigens.
- Null phenotypes are found in African, Indian, Chinese, Polynesian, and Finnish populations.
- The Jk(a)/Jk(b) polymorphism (c.838G>A) was identified in 1994.
Conclusions:
- The Kidd blood group system exhibits significant genetic diversity.
- Understanding JK gene variations is crucial for transfusion medicine and understanding null phenotypes.
- Further research into JK variants can improve serological diagnostics and patient care.
Abstract:
The Kidd blood group system has been recognized as clinically important in red blood cell (RBC) serology since its identification in 1951. Forty years later, the JK glycoprotein was determined to be a product of SCL14A1 and was identical to the urea transport protein UT-B produced by HUT11A. The functional role of the protein as a urea transporter in RBC and kidney has been well documented. The polymorphism responsible for the antithetical anigens Jk(a) and Jk(b) was identified in 1994 as c.838G>A (p.Asp280Asn). Recent discoveries have expanded the system to include 23 variant alleles recognized by the International Society of Blood Transfusion that silence the protein expression and 7 variant alleles presumably producting weak or partia JK antigens. Null phenotypes have been identified in individuals of several populations including those of African, Indian, and Chinese decent, in addition to the well-documented findings in the Polynesian and Finnish populations. This review will examine the historical information about the anigens and antibodies of the JK system as well as catalog the variations of the JK gene.
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