Biology:HLA-B58
From HandWiki
HLA-B (alpha)-β2MG with bound peptide | ||
major histocompatibility complex (human), class I, B58
| ||
Alleles | *5801, *5802 | |
Structure (See HLA-B) | ||
Shared data | ||
Locus | chr.6 6p21.31 |
HLA-B58 (B58) is an HLA-B serotype. B58 is a split antigen from the B17 broad antigen, the sister serotype B57.[1] The serotype identifies the more common HLA-B*58 gene products.[2] (For terminology help see: HLA-serotype tutorial) B*5801 is associated with allopurinol induced inflammatory necrotic skin disease.
Serotype
B*58 | B58 | B17 | Sample |
allele | % | % | size (N) |
Template:HBA | 79 | 4 | 2096 |
Template:HBA | 72 | 3 | 837 |
Allele distribution
freq | ||
ref. | Population | (%) |
[4] | Cameroon Pygmy Baka | 15.0 |
[4] | India Khandesh Pawra | 15.0 |
[4] | Cameroon Sawa | 11.5 |
[4] | Taiwan Hakka | 10.9 |
[4] | Kenya Nandi | 10.0 |
[4] | India West Bhils | 9.0 |
[4] | China South Han | 8.9 |
[4] | China Inner Mongolia | 8.8 |
[4] | India North Delhi | 8.8 |
[4] | Thailand Northeast | 8.4 |
[4] | Guinea Bissau | 7.8 |
[4] | Thailand | 7.7 |
[4] | India Mumbai Marathas | 7.4 |
[4] | India Andhra Pradesh Golla | 7.2 |
[4] | Kenya Luo | 7.0 |
[4] | Senegal Niokholo Mandenka | 6.9 |
[4] | India New Delhi | 6.8 |
[4] | Oman | 6.8 |
[4] | Russia Tuva (2) | 6.7 |
[4] | South Korea (3) | 6.5 |
[4] | Italy Sardinia (3) | 6.4 |
[4] | Burkina Faso Fulani | 6.1 |
[4] | Taiwan Siraya | 5.9 |
[4] | India North Hindus | 5.8 |
[4] | Burkina Faso Mossi | 5.7 |
[4] | Cameroon Yaounde | 5.4 |
[4] | Cameroon Bamileke | 5.2 |
[4] | Singapore Riau Malay | 5.0 |
[4] | Saudi Arabia Guraiat and Hail | 4.6 |
[4] | France Corsica | 4.5 |
[4] | Sudanese | 4.5 |
[4] | Zimbabwe Harare Shona | 4.4 |
[4] | Burkina Faso Rimaibe | 4.3 |
[4] | Iran Baloch | 4.0 |
[4] | South African Natal Zulu | 4.0 |
[4] | Tunisia | 4.0 |
[4] | Uganda Kampala | 4.0 |
[4] | Cameroon Beti | 3.7 |
[4] | Tunisia Ghannouch | 3.7 |
[4] | Taiwan Pazeh | 3.6 |
[4] | Tunisia Tunis | 3.4 |
[4] | Italy North (1) | 3.3 |
[4] | Israel Ashkenazi and Non Ashkenazi Jews | 3.2 |
[4] | India West Coast Parsis | 3.0 |
[4] | China North Han | 2.9 |
[4] | Ivory Coast Akan Adiopodoume | 2.3 |
[4] | Mali Bandiagara | 2.2 |
[4] | Mexico Zaptotec Oaxaca | 2.2 |
[4] | South Africa Natal Tamil | 2.0 |
[4] | China Yunnan Nu | 1.9 |
[4] | Bulgaria | 1.8 |
[4] | China Tibet Autonomous Region Tibetans | 1.6 |
[4] | France South East | 1.6 |
[4] | Israel Arab Druse | 1.5 |
[4] | Czech Republic | 1.4 |
[4] | Georgia Tbilisi Georgians | 1.4 |
[4] | Jordan Amman | 1.4 |
[4] | Morocco Nador Metalsa (berber) | 1.4 |
[4] | Croatia | 1.3 |
[4] | Romanian | 1.3 |
[4] | Spain Eastern Andalusia | 1.2 |
[4] | Australian Aborigine Cape York Peninsula | 1.0 |
B*5802 | ||
[4] | Cameroon Bamileke | 14.3 |
[4] | Kenya Luo | 12.5 |
[4] | Cameroon Yaounde | 10.9 |
[4] | Cameroon Pygmy Baka | 10.0 |
[4] | Cameroon Beti | 9.8 |
[4] | Kenya Nandi | 8.5 |
[4] | South African Natal Zulu | 8.5 |
[4] | Cameroon Sawa | 7.7 |
[4] | Zimbabwe Harare Shona | 6.4 |
[4] | Cape Verde Northwestern Islands | 5.6 |
[4] | Uganda Kampala | 4.4 |
[4] | Central Africa Republic Mbenzele Pygmy | 4.0 |
[4] | Zambia Lusaka | 2.3 |
[4] | Iran Baloch | 1.0 |
[4] | Tunisia | 1.0 |
Disease
HLA-B*5801 is involved in allopurinol sensitive drug induced Stevens–Johnson syndrome.[5][6] Allopurinol is a frequent cause of severe cutaneous adverse reactions, including drug-hypersensitivity syndrome, Stevens–Johnson syndrome, and toxic epidermal necrolysis (SJS/TEN).[7] The association with allopurinol sensitivity in SJS/TEN was extremely strong in Asia, and somewhat less associated in Europeans.[8]
References
- ↑ "The complete primary structure of HLA-Bw58". J. Biol. Chem. 260 (22): 11924–33. 1985. doi:10.1016/S0021-9258(17)38967-6. PMID 2995352.
- ↑ Marsh, S. G.; Albert, E. D.; Bodmer, W. F.; Bontrop, R. E.; Dupont, B.; Erlich, H. A.; Fernández-Viña, M.; Geraghty, D. E. et al. (2010). "Nomenclature for factors of the HLA system, 2010". Tissue Antigens 75 (4): 291–455. doi:10.1111/j.1399-0039.2010.01466.x. PMID 20356336.
- ↑ derived from IMGT/HLA
- ↑ 4.00 4.01 4.02 4.03 4.04 4.05 4.06 4.07 4.08 4.09 4.10 4.11 4.12 4.13 4.14 4.15 4.16 4.17 4.18 4.19 4.20 4.21 4.22 4.23 4.24 4.25 4.26 4.27 4.28 4.29 4.30 4.31 4.32 4.33 4.34 4.35 4.36 4.37 4.38 4.39 4.40 4.41 4.42 4.43 4.44 4.45 4.46 4.47 4.48 4.49 4.50 4.51 4.52 4.53 4.54 4.55 4.56 4.57 4.58 4.59 4.60 4.61 4.62 4.63 4.64 4.65 4.66 4.67 4.68 4.69 4.70 4.71 4.72 4.73 4.74 4.75 4.76 "New allele frequency database: http://www.allelefrequencies.net". Tissue Antigens 61 (5): 403–7. 2003. doi:10.1034/j.1399-0039.2003.00062.x. PMID 12753660.
- ↑ "Human leukocyte antigens and drug hypersensitivity". Curr Opin Allergy Clin Immunol 7 (4): 317–23. August 2007. doi:10.1097/ACI.0b013e3282370c5f. PMID 17620823.
- ↑ "Strong association between HLA-B*5801 and allopurinol-induced Stevens–Johnson syndrome and toxic epidermal necrolysis in a Thai population". Pharmacogenet Genomics 19 (9): 704–9. 2009. doi:10.1097/FPC.0b013e328330a3b8. PMID 19696695.
- ↑ Hung SI; Chung WH; Liou LB et al. (March 2005). "HLA-B*5801 allele as a genetic marker for severe cutaneous adverse reactions caused by allopurinol". Proc. Natl. Acad. Sci. U.S.A. 102 (11): 4134–9. doi:10.1073/pnas.0409500102. PMID 15743917. Bibcode: 2005PNAS..102.4134H.
- ↑ Lonjou C; Borot N; Sekula P et al. (February 2008). "A European study of HLA-B in Stevens–Johnson syndrome and toxic epidermal necrolysis related to five high-risk drugs". Pharmacogenet. Genomics 18 (2): 99–107. doi:10.1097/FPC.0b013e3282f3ef9c. PMID 18192896.
Original source: https://en.wikipedia.org/wiki/HLA-B58.
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