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Association of an HLA-DQ Allele with Clinical Tuberculosis

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Association of an HLA-DQ Allele with Clinical Tuberculosis Brief Report Association of an HLA-DQ Allele With Clinical Tuberculosis Anne E. Goldfeld, MD; Julio C. Delgado, MD; Sok Thim; M. Viviana Bozon, MD; Adele M. Uglialoro; David Turbay, MD; Carol Cohen; Edmond J. Yunis, MD Context.—Although tuberculosis (TB) is the leading worldwide cause of death clinical TB, we performed a 2-stage study due to an infectious disease, the extent to which progressive clinical disease is as- of molecular typing of HLA class I and sociated with genetic host factors remains undefined. class II alleles and also tested for the pres- α Objective.—To determine the distribution of HLA antigens and the frequency of ence of 2 TNF- alleles in Cambodian pa- 2 alleles of the tumor necrosis factor a (TNF-a) gene in unrelated individuals with tients with clinical TB and in control indi- viduals who did not have a history of TB. clinical TB (cases) compared with individuals with no history of clinical TB (controls) in a population with a high prevalence of TB exposure. Methods Design.—A 2-stage, case-control molecular typing study conducted in 1995-1996. The study subjects were unrelated Cam- Setting.—Three district hospitals in Svay Rieng Province in rural Cambodia. bodian patients recruited from a TB treat- Patients.—A total of 78 patients with clinical TB and 49 controls were included ment program in eastern rural Cambodia. in the first stage and 48 patients with TB and 39 controls from the same area and Two different groups of patients and con- socioeconomic status were included in the second stage. trols were recruited for the 2 stages of the Main Outcome Measures.—Presence of HLA class I and class II alleles deter- study, the first group in 1995 and the sec- mined by sequence-specific oligonucleotide probe hybridization and presence of 2 ond group in 1996. The patients were ran- TNF-a alleles determined by restriction fragment length polymorphism analysis. domly selected from all inpatients or out- Results.—In the first stage, 7 DQB1*0503 alleles were detected among 156 al- patients picking up their monthly supply of TB medicines at Chantrea, Rumduol, or leles derived from patients with TB, whereas no DQB1*0503 alleles were found among the 98 alleles derived from controls (P=.04). There was no detectable dif- Kompong Rho District Hospitals in Svay Rieng Province. ference in the distribution of the 2 TNF-a alleles in patients with TB compared with The diagnosis of clinical TB was made controls. In the second stage, we tested for the presence of a single variable, the on site on the basis of light microscopy DQB1*0503 allele, and found 9 DQB1*0503 alleles among 96 alleles derived from demonstrating the presence of acid-fast patients with TB and no DQB1*0503 alleles among 78 alleles in controls (P=.005). bacilli in sputum, pleural fluid, or lymph Conclusions.—The HLA-DQB1*0503 allele is significantly associated with sus- node drainage. One of us (S.T.) conducted ceptibility to TB in Cambodian patients and, to our knowledge, is the first identified family interviews of the household mem- gene associated with development of clinical TB. bers of the patients and verified that no JAMA. 1998;279:226-228 patients in the study were related. Con- trol individuals were recruited from pa- ABOUT A THIRD of the earth’s popula- quired immunodeficiency syndrome tients visiting the same hospitals for mi- tion is infected with Mycobacterium tu- (AIDS) have a greatly increased risk of nor complaints. Based on detailed clinical berculosis,1-3 the bacteria that causes activation of quiescent infection with M history, controls did not have a history of tuberculosis (TB). Infection with M tuber- tuberculosis .4-6 Poverty also has been im- TB or current symptoms consistent with culosis results in a variety of conditions plicated as a cofactor in disease progres- TB. All patients and controls were fol- ranging from asymptomatic infection to sion.7,8 Certain populations are at risk for lowed up for 6 months to confirm their progressive pulmonary or extrapulmo- increased susceptibility to infection and diagnosis or control status. nary TB and death.4 Approximately 1 in progressive disease due to M tuberculo- After consent was obtained, blood was 10 of those infected will progress to ac- sis,9-13 and in several populations the HLA drawnfromeachsubjectandstoredat4°C tive disease during their lifetime.1-3 Tu- class II DR2 serotype is associated with for 4 to 10 days. Plasma and peripheral berculosis is the leading cause of death due clinical TB.11-13 Mutations in the inter- blood mononuclear cells (PBMCs) were to an infectious disease worldwide, ac- feron-g receptor gene have been associ- prepared according to standard tech- counting for approximately 3 million ated with progressive atypical mycobac- niques and stored at −70°C. Plasma deaths annually.1-3 terial infection14 and with Calmette- sampleswerescreenedforevidenceofan- Individuals who have impaired cell- Gue´rin bacillus (Mycobacterium bovis) tibodies to human immunodeficiency vi- mediated immunity due to chemo- infection.15 Tumor necrosis factor a (TNF- rus (HIV) types 1 and 2 and human T- therapy, steroid use, neoplasia, or the ac- a) appears to play an important role in lymphotropic virus (HTLV) types 1 and 2 TB pathogenesis, including granuloma by enzyme-linked immunosorbent assay. From the Divisions of Adult Oncology (Dr Goldfeld and formation and containment of TB infec- The DNA was prepared from PBMCs Ms Uglialoro) and Immunogenetics (Drs Delgado, Bo- tion16,17 and impaired TNF-a secretion by a quick isolation method,18 and allele- zon, Turbay, and Yunis) and the Blood Bank (Ms Cohen), Dana-Farber Cancer Institute, Boston, Mass, and the due to defective signaling through the in- specific polymerase chain reaction (PCR) Cambodian Health Committee, Phnom Penh (Mr Sok). terferon-g receptor gene may be in- was performed. For HLA class I typing, Reprints: Anne E. Goldfeld, MD, Division of Adult volved in disease progression.14,15 PCR amplification of exons 2 and 3 of the Oncology, Dana-Farber Cancer Institute, 44 Binney St, Boston, MA 02115 (e-mail: anne_goldfeld@ To determine whether specific HLA HLA-A and HLA-B loci was performed. macmailgw.dfci.harvard.edu). class I or class II alleles are associated with For class II typing, PCR amplification of 226 JAMA, January 21, 1998—Vol 279, No. 3 HLA-DQ and Tuberculosis—Goldfeld et al ©1998 American Medical Association. All rights reserved. Downloaded From: https://jamanetwork.com/ on 10/01/2021 exon 2 of the HLA-DRB, DQB1, and DQA1 (Table). HLA-B38 was present in 16 of 138 Frequencies of Major Histocompatibility Complex loci was performed.19-21 The PCR prod- alleles among patients with TB com- (MHC) Class II Antigens in Patients With Tubercu- ucts were separated by agarose gel elec- pared with 2 of 96 alleles in controls losis (TB) and Control Individuals From Cambodia* trophoresis, stained with ethidium bro- (P=.005) (data not shown). TB, Controls, mide, and photographed. Dot-blot, An RFLP analysis scoring for the 2 No. (%) No. (%) P prehybridization, and hybridization pro- TNF-α promoter variants revealed 11 Allele (n=156†) (n=98†) Value cedures were carried out according to the TNF2 alleles of 156 alleles derived from DRB1 1501 12 (7.7) 7 (7.1) .99 manufacturer’s instructions (Lifecodes patients with TB and 8 TNF2 alleles of 1502 26 (16.7) 18 (18.4) .74 Corp, Stamford, Conn). Class I and class 96 alleles derived from controls with no II alleles were identified in the PCR- difference in TNF2 variant expression 1602 14 (9.0) 7 (7.1) .65 amplified products by sequence-specific oli- in either group. Seventeen of the 19 0301 14 (9.0) 11 (11.2) .67 gonucleotide probe hybridization.20,22-25 TNF2 alleles were found in HLA-DR3– 0403 1 (0.6) 0 .99 TheTNF-αalleles were determined by positivesubjects(datanotshown).Thus, 0404 1 (0.6) 0 .99 restriction fragment length polymor- as in other populations,26 the TNF2 al- 0405 5 (3.2) 7 (7.1) .22 phism (RFLP) analysis using primers de- lele was in linkage disequilibrium with 0406 1 (0.6) 1 (1) .16 signed to incorporate a polymorphic site HLA-DR3. 1101 4 (2.6) 2 (2) .99 (the nucleotide A vs G) at position −308 Based on the first stage of our analy- 1106 0 2 (2) .15 nucleotides (nt) relative to the TNF-α sis, we chose to further investigate the as- 1201 2 (1.3) 0 .52 transcription start site. The TNF2 (A at sociation of the single class II allele, 1202 23 (14.7) 17 (17.3) .60 −308 nt) polymorphism creates an NcoI DQB1*0503, and TB. This second stage in- 1301 2 (1.3) 0 .52 restriction site and can be differentiated cluded 48 patients with pulmonary TB 1302 1 (0.6) 1 (1) .16 by size (107 nt for the TNF1 and 87 nt for (mean age, 46 years; range, 25-76 years; 1312 2 (1.3) 0 .52 the TNF2 allele) from the TNF1 allele by 40% male) and 39 controls (mean age, 40 1401 7 (4.5) 5 (5.1) .99 26 agarose gel electrophoresis. years; range, 19-67 years; 30% male). One 1404 5 (3.2) 0 .16 The frequencies of independent HLA control subject tested positive for anti- 1405 1 (0.6) 0 .99 α alleles and TNF- alleles in patients bodies to HIV-1 and was excluded from 1407 3 (1.9) 1 (1) .99 and controls were determined by direct the HLA analysis. Among the 96 alleles 0701 12 (7.7) 9 (9.2) .81 counting.
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