HLA-A24

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major histocompatibility complex (human), class I, A24
Alleles A*2402
A*2403
Structure (See HLA-A)
Identifiers
2402 2403
Symbol(s) HLA-A
EBI-HLA A*2402
Shared data
Locus chr.6 6p21.31

HLA-A24 (A24) is an HLA-A serotype. The serotype identifies the more common HLA-A*24 gene products. A24 is a split antigen that is also recognized by the A9 broad antigen type. This broad antigen also recognizes the similar A23 types. A24 is common in Austronesia. A*2402 has one of the highest A allele frequencies for a number of peoples, including Papua New Guineans, Indigeonous Taiwanese (Eastern Tribals), Yupik and Greenland Eskimos. It is common over much of Southeastern Asia. In eurasia it is least common in Ireland, and it is relatively uncommon in Africa except North Africa and Kenya.


Serotype

A24 and A9 serotype recognition of Some HLA A*24 allele-group gene products[1]
A*24 A24 A9 Sample
allele  %  % size (N)
2402 97 3098
2402 55 4 282


There are over 90 known A*24 alleles, 69 code for different isoforms and 7 are nulls.

Disease Associations

By serotype

A24 has a secondary risk factor for myasthenia gravis,,[2] Buerger's disease[3]

By allele

A*2402 is a secondary risk factor,[4] alters type 1 diabetes risk,[5][6] and allele associated with thyomoma induced myasthenia gravis.

A24-B Haplotypes

HLA A24-B35 haplotype by Cw frequencies
freq Rank in
ref. Population (%) Pop.
[7] Java (Indonesia) 8.0 1 4
[7] S. Amer. Native 6.3 1 3
[7] N. Amer. Native 5.4 1 5
[7] Mexican 4.7 1
[7] Inuit 4.2 1
[7] Brazilian 3.8 1
[7] Austria 3.5 1
[7] Portuguese 3.1 1 3
[7] Yakut 2.9 1
[7] Mongolian 2.7 1
[7] Timor 2.5 1 5
[7] Bharghavas (India) 2.4 1
[7] Greek 2.3 1
[7] Italian 2.2 1
[7] Mongolian 1.9 1
[7] Vietnamese 1.8 1
[7] Japanese 1.6 2
[7] French 1.2 2
1 Cw4. 2 Cw9.

A24-Cw7-B39
A24-Cw10-B60
A24-Cw10-B61
A24-B48

A24-Cw4-B35

This particular haplotype is common across a fairly wide region, possibly the most widely spread A-Cw-B haplotype in humans. Cw4-B35 has a node within the region once referred to as Thracia/Dacia.

A24-Cw*14-B51

HLA A24-CBL-B51 (CBL=1402) haplotype frequencies
freq
ref. Population (%)
[7] Korean 3.5
[7] Iyers 3.4
[7] Mongolian 2.9
[7] Japanese 2.6
[7] Romanian 2.2
[7] Greek 2.1
[7] Hungarian 2.0
[7] Italian 0.6

References

  1. derived from IMGT/HLA
  2. Machens A, Löliger C, Pichlmeier U, Emskötter T, Busch C, Izbicki J (1999). "Correlation of thymic pathology with HLA in myasthenia gravis.". Clin Immunol 91 (3): 296-301. PMID 10370374.
  3. Numano F, Sasazuki T, Koyama T, Shimokado K, Takeda Y, Nishimura Y, Mutoh M (1986). "HLA in Buerger's disease.". Exp Clin Immunogenet 3 (4): 195-200. PMID 3274054.
  4. de Juan M, Reta A, Belzunegui J, Figueroa M, Maruri N, Cuadrado E (2004). "HLA-A*2402 and a microsatellite (D6S248) are secondary independent susceptibility markers to ankylosing spondylitis in Basque patients.". Hum Immunol 65 (2): 175-80. PMID 14969772.
  5. Noble J, Valdes A, Bugawan T, Apple R, Thomson G, Erlich H (2002). "The HLA class I A locus affects susceptibility to type 1 diabetes.". Hum Immunol 63 (8): 657-64. PMID 12121673.
  6. Nakanishi K, Inoko H (2006). "Combination of HLA-A24, -DQA1*03, and -DR9 Contributes to Acute-Onset and Early Complete {beta}-Cell Destruction in Type 1 Diabetes: Longitudinal Study of Residual {beta}-Cell Function.". Diabetes 55 (6): 1862-8. PMID 16731854.
  7. 7.00 7.01 7.02 7.03 7.04 7.05 7.06 7.07 7.08 7.09 7.10 7.11 7.12 7.13 7.14 7.15 7.16 7.17 7.18 7.19 7.20 7.21 7.22 7.23 7.24 7.25 Sasazuki, Takehiko; Tsuji, Kimiyoshi; Aizawa, Miki (1992). HLA 1991: proceedings of the eleventh International Histocompatibility Workshop and Conference, held in Yokohama, Japan, 6-13 November, 1991. Oxford [Oxfordshire]: Oxford University Press. ISBN 0-19-262390-7. 
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Acknowledgement and Attribution Regarding Sources of Content

Some of the initial content on this page may be incorporated in part from copyleft sources in the public domain including wikis such as Wikipedia and AskDrWiki. Drug information for patients came from the The National Library of Medicine. Infectious disease information may have come from the Centers for Disease Control (CDC). Differential Diagnoses are drawn from clinicians as well as an amalgamation of 3 sources: 1.The Disease Database; 2. Kahan, Scott, Smith, Ellen G. In A Page: Signs and Symptoms. Malden, Massachusetts: Blackwell Publishing, 2004:3; 3. Sailer, Christian, Wasner, Susanne. Differential Diagnosis Pocket. Hermosa Beach, CA: Borm Bruckmeir Publishing LLC, 2002:7 .

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