Condition Related References

Evans DM et al. Interaction between ERAP1 and HLA-B27 in ankylosing spondylitis implicates peptide handling in the mechanism for HLA-B27 in disease susceptibility. Nat Genet. 2011; 43:761.
Granfors K et al. The cutting edge of spondylarthropathy research in the millennium. Arthritis Rheum. 2002; 46:606.
Reveille JD. Genetics of spondyloarthritis–beyond the MHC. Nat Rev Rheumatol. 2012; 8:296.
Reveille JD. Recent studies on the genetic basis of ankylosing spondylitis. Curr Rheumatol Rep. 2009; 11:340.
Uchanska-Ziegler B et al. Structural and dynamic features of HLA-B27 subtypes. Curr Opin Rheumatol. 2013; 25:411.

Hershfield MS, Callaghan JT, Tassaneeyakul W, et al. Clinical Pharmacogenetics Implementation Consortium guidelines for human leukocyte antigen-B genotype and allopurinol dosing. Clin Pharmacol Ther. 2013;93(2):153-8.
Saito Y, Stamp LK, Caudle KE, et al. Clinical Pharmacogenetics Implementation Consortium (CPIC) guidelines for human leukocyte antigen B (HLA-B) genotype and allopurinol dosing: 2015 update. Clin Pharmacol Ther. 2016;99(1):36-7.
Yu KH, Yu CY, Fang YF. Diagnostic utility of HLA-B*5801 screening in severe allopurinol hypersensitivity syndrome: an updated systematic review and meta-analysis. Int J Rheum Dis. 2017;20(9):1057-1071..

Megiorni F et al. HLA-DQ and risk gradient for celiac disease. Hum Imm. 2009; 70:55-59.
Megiorni F et al. HLA-DQA1 and HLA-DQB1 in celiac disease predisposition: practical implications of the HLA molecular typing. J of Biomed Sci. 2012; 19:88.
Abadie et al. Integration of genetic and immunological insights into a model of celiac disease pathogenesis. Annu. Rev. Immunol. 2011; 29:493-525.
Kagnoff MF. Celiac disease: pathogenesis of a model immunogenetic disease. J Clin Invest. 2007; 117:41-49.
Megiorni F et al. HLA-DQ and susceptibility to celiac disease: evidence for gender differences and parent-of-origin effects. Am J Gastroenterol. 2008; 103:997-1003.
Karell et al. HLA types in celiac disease patients not carrying the DQA1*05-DQB1*02(DQ2) heterodimer: results from the European genetics cluster of celiac disease. Hum Immunol. 2003; 64:469-477

Gray MR, Thrasher JD, Crago R, et al. Mixed mold mycotoxicosis: immunological changes in humans following exposure in water-damaged buildings. Arch Environ Health. 2003;58(7):410-20.
Vlachopoulou E, Lahtela E, Wennerström A, et al. Evaluation of HLA-DRB1 imputation using a Finnish dataset. Tissue Antigens. 2014;83(5):350-5.
Empting LD. Neurologic and neuropsychiatric syndrome features of mold and mycotoxin exposure. Toxicol Ind Health. 2009;25(9-10):577-81.
Kilburn KH. Neurobehavioral and pulmonary impairment in 105 adults with indoor exposure to molds compared to 100 exposed to chemicals. Toxicol Ind Health. 2009;25(9-10):681-92.
Knutsen AP, Vijay HM, Kumar V, et al. Mold-sensitivity in children with moderate-severe asthma is associated with HLA-DR and HLA-DQ. Allergy. 2010;65(11):1367-75.

Banwell BL. Pediatric multiple sclerosis. Curr Neurol Neurosci Rep. 2004; 4:245.
Friese MA et al. Opposing effects of HLA class I molecules in tuning autoreactive CD8+ T cells in multiple sclerosis. Nat Med. 2008; 14:1227.
Lincoln MR et al. A predominant role for the HLA class II region in the association of the MHC region with multiple sclerosis. Nat Genet. 2005; 37:1108.
Nolan D et al. Contributions of vitamin D response elements and HLA promoters to multiple sclerosis risk. Neurology. 2012; 79:538.
Ramagopalan SV et al. Expression of the multiple sclerosis-associated MHC class II Allele HLA-DRB1*1501 is regulated by vitamin D. PLoS Genet. 2009; 5:e1000369.
Renoux C et al. Natural history of multiple sclerosis with childhood onset. N Engl J Med. 2007; 356:2603.

Krebs, Kristi, et al. Genome-wide Study Identifies Association between HLA-B∗ 55: 01 and Self-Reported Penicillin Allergy. The American Journal of Human Genetics (2020).

Arnett FC. Histocompatibility typing in the rheumatic diseases. Diagnostic and prognostic implications. Rheum Dis Clin North Am. 1994; 20:371.
Cruz-Tapias P et al. HLA and Sjögren’s syndrome susceptibility. A meta-analysis of worldwide studies. Autoimmun Rev. 2012 Feb;11(4):281-7.
Bolstad AI et al. HLA markers and clinical characteristics in Caucasians with primary Sjögren’s syndrome. J Rheumatol. 2001; 28:1554.
Kang HI et al. Comparison of HLA class II genes in Caucasoid, Chinese, and Japanese patients with primary Sjögren’s syndrome. J Immunol. 1993; 150:3615.
Mattey DL et al. Association between HLA-DRB1*15 and secondary Sjögren’s syndrome in patients with rheumatoid arthritis. J Rheumatol. 2000; 27:2611.
Takahashi M et al. HLA and CTLA4 polymorphisms may confer a synergistic risk in the susceptibility to Graves’ disease. J Hum Genet. 2010; 55:323.
El Miedany YM. Hyperprolactinemia in Sjogren’s syndrome: a patient subset or a disease manifestation? Joint Bone Spine. 2004 May; 71(3):203-8.

Barcellos LF et al. High-density SNP screening of the major histocompatibility complex in systemic lupus erythematosus demonstrates strong evidence for independent susceptibility regions. PLoS Genet. 2009; 5:e1000696.
Danchenko N et al. Epidemiology of systemic lupus erythematosus: a comparison of worldwide disease burden. Lupus. 2006; 15:308.
Galeazzi M et al. Anti-ganglioside antibodies in a large cohort of European patients with systemic lupus erythematosus: clinical, serological, and HLA class II gene associations. European Concerted Action on the Immunogenetics of SLE. J Rheumatol. 2000; 27:135.
International MHC and Autoimmunity Genetics Network, Rioux JD et al. Mapping of multiple susceptibility variants within the MHC region for 7 immune-mediated diseases. Proc Natl Acad Sci U S A. 2009; 106:18680.

At-Home Tests