HLA-DR and HLA-DQ Alleles in Patients from the South of Brazil: Markers for Leprosy Susceptibility and Resistance
Overview
Authors
Affiliations
Background: Many epidemiological studies have shown that the genetic factors of the host play a role in the variability of clinical response to infection caused by M. leprae. With the purpose of identifying genes of susceptibility, the present study investigated the possible role of HLA-DRB1 and DQA1/DQB1 alleles in susceptibility to leprosy, and whether they account for the heterogeneity in immune responses observed following infection in a Southern Brazilian population.
Methods: One hundred and sixty-nine leprosy patients and 217 healthy controls were analyzed by polymerase chain reaction amplification and reverse hybridization with sequence-specific oligonucleotide probes and sequence-specific primers (One Lambda, CA, USA).
Results: There was a positive association of HLA-DRB1*16 (*1601 and *1602) with leprosy per se (7.3% vs. 3.2%, P = 0.01, OR = 2.52, CI = 1.26-5.01), in accord with previous serological studies, which showed DR2 as a marker of leprosy. Although, HLA-DQA1*05 frequency (29.8% vs. 20.9%, P = 0.0424, OR = 1.61, CI = 1.09-2.39) was higher in patients, and HLA-DQA1*02 (3.0% vs. 7.5%, P = 0.0392, OR = 0.39, CI = 0.16 - 0.95) and HLA-DQA1*04 (4.0% vs. 9.1%, P = 0.0314, OR = 0.42, CI = 0.19 - 0.93) frequencies lower, P-values were not significant after the Bonferroni's correction. Furthermore, HLA-DRB1*1601 (9.0% vs. 1.8%; P = 0.0016; OR = 5.81; CI = 2.05-16.46) was associated with susceptibility to borderline leprosy compared to control group, and while HLA-DRB1*08 (11.2% vs. 1.2%; P = 0.0037; OR = 12.00; CI = 1.51 - 95.12) was associated with susceptibility to lepromatous leprosy, when compared to tuberculoid leprosy, DRB1*04 was associated to protection.
Conclusion: These data confirm the positive association of HLA-DR2 (DRB1*16) with leprosy per se, and the protector effect of DRB1*04 against lepromatous leprosy in Brazilian patients.
Psoriasis and Leprosy: An Arcane Relationship.
Ge G, Shang J, Gan T, Chen Z, Pan C, Mei Y J Inflamm Res. 2023; 16:2521-2533.
PMID: 37337513 PMC: 10277007. DOI: 10.2147/JIR.S407650.
CD4+ Cytotoxic T Cells Involved in the Development of EBV-Associated Diseases.
Ruiz-Pablos M Pathogens. 2022; 11(8).
PMID: 35894054 PMC: 9330826. DOI: 10.3390/pathogens11080831.
Gene Expression Profile of Contribution in the Pathology of Leprosy Neuropathy.
de Souza B, Mendes M, da Silva G, Sammarco-Rosa P, de Moraes M, Jardim M Front Med (Lausanne). 2022; 9:861586.
PMID: 35492305 PMC: 9051340. DOI: 10.3389/fmed.2022.861586.
Teles S, Silva E, de Souza R, Tomimori J, Florian M, Souza R Braz J Infect Dis. 2020; 24(4):296-303.
PMID: 32589879 PMC: 9392080. DOI: 10.1016/j.bjid.2020.05.009.
Human Genetic Susceptibility of Leprosy Recurrence.
Uaska Sartori P, Penna G, Buhrer-Sekula S, Pontes M, Goncalves H, Cruz R Sci Rep. 2020; 10(1):1284.
PMID: 31992776 PMC: 6987179. DOI: 10.1038/s41598-020-58079-3.