HLA-A24

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Further information: HLA serotypes explained
HLA-A24
(MHC Class I, A cell surface antigen)
Rendering of 2bck​: α (A*2402 gene product), β2-microglobulin, and telomerase peptide.
About
Proteintransmembrane receptor/ligand
Structureαβ heterodimer
SubunitsHLA-A*24--, β2-microglobulin
Older namesHL-A9
Subtypes
Subtype
allele
Available structures
A24 *2402 2bck​
A9.3 *2403
Alleles link-out to IMGT/HLA database at EBI

HLA-A24 (A24) is a human leukocyte antigen serotype within HLA-A serotype group. The serotype is determined by the antibody recognition of α24 subset of HLA-A α-chains. For A24, the alpha, "A", chain are encoded by the HLA-A*24 allele group and the β-chain are encoded by B2M locus.[1] This group currently is dominated by A*2402. A24 and A*24 are almost synonymous in meaning. A24 is a split antigen of the broad antigen HLA-A9 and it is a sister serotype of HLA-A23.

A*2402 has one of the highest "A" frequencies identified for a number of peoples, including Papua New Guineans, Indigenous Taiwanese (Eastern Tribals), Yupik and Greenland [Aleuts]. It is common over much of Southeastern Asia. In Eurasia it is least common in Ireland, and A24 is relatively uncommon in Africa except North Africa and Kenya.

Serotype

[edit]
A24 recognition of some HLA A*24 gene products[2]
A*24 A24 A9 Sample
allele % % size (N)
*2402 97 3098
*2403 55 4  282

There are over 90 known A*24 alleles, 69 code for different isoforms and 7 are nulls. A*2403 can also be detected as A2403 serotype.

Associated disease

[edit]

A24 has a secondary risk factor for myasthenia gravis,[3] Buerger's disease.[4] It is also associated with Type 1 Diabetes (T1D)[5][6] and systemic lupus erythematosus (SLE)[7].

Alleles

[edit]
HLA A*2402 frequencies
Study populationFreq.
 (in %)[8]
Taiwan Paiwan86.3
Taiwan Tsou78.4
Taiwan Rukai76.0
Papua New Guinea Goroka74.4
PNG Karimui Plateau74.4
Taiwan Puyuma64.0
Taiwan Ami62.8
PNG Wanigela62.7
Taiwan Atayal61.8
Ecuador Cayapa61.4
New Caledonia60.7
Venezuela Perja Mtn. Bari60.2
USA Alaska Yupik Natives58.1
Taiwan Tao54.0
PNG Wosera51.3
Taiwan Siraya47.1
Taiwan Taroko44.5
Mexico Chihuahua Tarahuma…37.5
USA Arizona Pima36.0
Taiwan Pazeh33.6
Japan Okinawa Ryukyuan33.5
American Samoa33.0
Japan (5)32.7
Philippines Ivatan32.0
PNG New Britain Rabaul31.6
N. Mexico Canoncito Navaj…30.5
Australia Indig. Yuendumu29.8
Australia Indig. Groote E…29.3
China Tibetans27.2
S. Dakota Lakota Sioux26.2
Mexico Mixtec Oaxaca24.5
Japan Ainu Hokkaido24.0
Venezuela Perija Mtns. Yu…23.3
Mexico Zaptotec Oaxaca23.1
USA North American Native…22.7
Australia Indig. Cape Yor…22.3
Ch. Guangdong Meizhou Han22.2
Russia Tuva (2)21.5
Singapore Chinese Han21.5
India North Hindus20.2
Mongolia Buriat20.0
China Inner Mongolia19.6
USA Asian18.9
Taiwan Minnan (1)18.6
China South Han17.2
Georgia Tbilisi Georgian…17.1
India Mumbai Marathas16.7
Mexico Guadalajara Mestiz…16.5
Singapore Riau Malay16.5
Croatia16.0
India Khandesh Pawra16.0
Singapore Javanese Indone…16.0
South Africa Natal Tamil16.0
India Tamil Nadu Nadar15.6
PNG Madang15.3
China North Han15.2
USA South Texas Hispanics15.2
PNG West Schrader Ranges14.2
China Guangxi Maonan13.4
Mexico Mestizos13.4
Georgia Svaneti Svans13.1
Romanian12.7
Pakistan Burusho12.5
USA Hispanic12.2
Bulgaria11.8
Georgia Tbilisi Kurds11.7
India New Delhi11.4
Pakistan Sindhi10.7
USA Caucasian10.7
France South East10.6
Pakistan Pathan10.2
Cameroon Pygmy Baka10.0
Finland9.4
Brazil8.6
Australia Indig. Kimberly8.3
Australia New South Wales8.2
Israel Arab Druse8.0
Pakistan Baloch8.0
Portugal Centre8.0
Cameroon Sawa7.7
Brazil Terena7.5
Ireland South6.8
Tunisia6.7
Belgium6.6
Morocco Berber Nador Meta…6.2
Jordan Amman5.9
Oman5.9
Mexico Mixe Oaxaca5.7
Portugal North5.4
Sudanese5.3
Mexico Sonora Seri4.5
Uganda Kampala4.3
Thailand3.9
Iran Baloch3.4
USA African America2.8
Kenya2.1
Guinea Bissau1.5
Czech Republic1.0
Kenya Nandi1.0
Allele frequencies presented, only

A*2402 is a secondary risk factor,[9] alters type 1 diabetes risk,[10][11] and allele associated with thymoma-induced myasthenia gravis.

Haplotypes

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

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

A24-Cw4-B35

[edit]

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

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

References

[edit]
  1. ^ Arce-Gomez B, Jones EA, Barnstable CJ, Solomon E, Bodmer WF (February 1978). "The genetic control of HLA-A and B antigens in somatic cell hybrids: requirement for beta2 microglobulin". Tissue Antigens. 11 (2): 96–112. doi:10.1111/j.1399-0039.1978.tb01233.x. PMID 77067.
  2. ^ Allele Query Form IMGT/HLA - European Bioinformatics Institute
  3. ^ Machens A, Löliger C, Pichlmeier U, Emskötter T, Busch C, Izbicki JR (June 1999). "Correlation of thymic pathology with HLA in myasthenia gravis". Clinical Immunology. 91 (3): 296–301. doi:10.1006/clim.1999.4710. PMID 10370374.
  4. ^ Numano F, Sasazuki T, Koyama T, Shimokado K, Takeda Y, Nishimura Y, Mutoh M (1986). "HLA in Buerger's disease". Experimental and Clinical Immunogenetics. 3 (4): 195–200. PMID 3274054.
  5. ^ Adamashvili I, McVie R, Gelder F, Gautreaux M, Jaramillo J, Roggero T, McDonald J (July 1997). "Soluble HLA class I antigens in patients with type I diabetes and their family members". Human Immunology. 55 (2): 176–83. doi:10.1016/S0198-8859(97)00096-7. PMID 9361970.
  6. ^ Kronenberg D, Knight RR, Estorninho M, Ellis RJ, Kester MG, de Ru A, Eichmann M, Huang GC, Powrie J, Dayan CM, Skowera A, van Veelen PA, Peakman M (July 2012). "Circulating preproinsulin signal peptide-specific CD8 T cells restricted by the susceptibility molecule HLA-A24 are expanded at onset of type 1 diabetes and kill β-cells". Diabetes. 61 (7): 1752–9. doi:10.2337/db11-1520. PMC 3379678. PMID 22522618.
  7. ^ Adamashvili I, Wolf R, Aultman D, Milford EL, Jaffe S, Hall V, Pressly T, Minagar A, Kelley R (November 2003). "Soluble HLA-I (s-HLA-I) synthesis in systemic lupus erythematosus". Rheumatology International. 23 (6): 294–300. doi:10.1007/s00296-003-0306-3. PMID 12879264.
  8. ^ Middleton, D.; Menchaca, L.; Rood, H.; Komerofsky, R. (2003). "New allele frequency database: http://www.allelefrequencies.net". Tissue Antigens. 61 (5): 403–407. doi:10.1034/j.1399-0039.2003.00062.x. PMID 12753660.
  9. ^ de Juan MD, Reta A, Belzunegui J, Figueroa M, Maruri N, Cuadrado E (February 2004). "HLA-A*2402 and a microsatellite (D6S248) are secondary independent susceptibility markers to ankylosing spondylitis in Basque patients". Human Immunology. 65 (2): 175–80. doi:10.1016/j.humimm.2003.11.006. PMID 14969772.
  10. ^ Noble JA, Valdes AM, Bugawan TL, Apple RJ, Thomson G, Erlich HA (August 2002). "The HLA class I A locus affects susceptibility to type 1 diabetes". Human Immunology. 63 (8): 657–64. doi:10.1016/S0198-8859(02)00421-4. PMC 4049513. PMID 12121673.
  11. ^ Nakanishi K, Inoko H (June 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. doi:10.2337/db05-1049. PMID 16731854.
  12. ^ a b c d e f g h i j k l m n o p q r s t u v w x y z 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 978-0-19-262390-4.
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