Leprosy in a high‐prevalence Egyptian village: epidemiology and risk factors

Hegazy, A. A.; Abdel‐Hamid, Ibrahim A.; Ahmed, El‐Shahat F.; Hammad, Sabry Mohamed; Hawas, Samia

doi:10.1046/j.1365-4362.2002.01602.x

Cited by 25 publications

(22 citation statements)

References 13 publications

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“…The association of HLA-DR2 (now DRB1*15 and DRB1*16) with susceptibility to leprosy per se has been highlighted in other studies [24,25] and in LL and TT patients, compared to healthy controls, in many populations around the world (Surinam, India, Venezuela, Egypt, Chine, Japan, Korea, Mexico, Turkey, Brazil) [reviewed in [12,26]]. Associations with the class II region are thought to occur due to the class II restriction of the presentation of mycobacterial epitopes to T-helper cells.…”

Section: Discussionmentioning

confidence: 78%

HLA-DR and HLA-DQ alleles in patients from the south of Brazil: markers for leprosy susceptibility and resistance

et al. 2009

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BackgroundMany 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.MethodsOne 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).ResultsThere 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.ConclusionThese 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.

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Section: Discussionmentioning

confidence: 78%

HLA-DR and HLA-DQ alleles in patients from the south of Brazil: markers for leprosy susceptibility and resistance

et al. 2009

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“…Moreover, patients with DR2 were more likely to have persistently positive ANCA. HLA-DR2 has been associated also with multiple sclerosis,25 anti-GBM disease,26 and other chronic granulomatous diseases such as sarcoidosis27 and leprosy 28. An interesting case study reported a young boy homozygous for HLA-DR2 who developed anti-GBM disease coincident with ulcerative colitis 29.…”

Section: Discussionmentioning

confidence: 99%

ANCA patients have T cells responsive to complementary PR-3 antigen

Yang

Bautz

Lionaki

et al. 2008

Kidney International

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Some patients with proteinase 3 specific anti-neutrophil cytoplasmic autoantibodies (PR3-ANCA) also have antibodies that react to complementary-PR3 (cPR3), a protein encoded by the antisense RNA of the PR3 gene. To study whether patients with anti-cPR3 antibodies have cPR3-responsive memory T cells we selected conditions that allowed cultivation of memory cells but not naïve cells. About half of the patients were found to have CD4+TH1 memory cells responsive to the cPR3138-169-peptide; while only a third of the patients had HI-PR3 protein responsive T cells. A significant number of T cells from patients responded to cPR3138-169 peptide and to HI-PR3 protein by proliferation and/or secretion of IFN-γ, compared to healthy controls while there was no response to scrambled peptide. Cells responsive to cPR3138-169-peptide were not detected in MPO-ANCA patients suggesting that this response is specific. The HLADRB1* 15 allele was significantly overrepresented in our patient group and is predicted to bind cPR3138-169 peptide with high affinity. Regression analysis showed a significant likelihood that anti-cPR3 antibodies and cPR3-specific T cells coexist in individuals, consistent with an immunological history of encounter with a PR3-complementary protein. We suggest that the presence of cells reacting to potential complementary protein pairs might provide an alternative mechanism for auto-immune diseases.

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“…The HLA-DR2 molecule [12, 13, 15, 21–24, 29, 32], later identified as DRB1 * 15 and DRB1 * 16 variants, is primarily associated with leprosy (LD or different clinical forms) in Indian, Japanese, Brazilian, and Chinese patients [25–27, 30, 33, 35, 36, 38, 39, 42]. …”

Section: Classical Hla Class II Genesmentioning

confidence: 99%

Role ofHLA,KIR,MICA, and Cytokines Genes in Leprosy

Jarduli

Sell

Reis

et al. 2013

BioMed Research International

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Many genes including HLA, KIR, and MICA genes, as well as polymorphisms in cytokines have been investigated for their role in infectious disease. HLA alleles may influence not only susceptibility or resistance to leprosy, but also the course of the disease. Some combinations of HLA and KIR may result in negative as well as positive interactions between NK cells and infected host cells with M. leprae, resulting in activation or inhibition of NK cells and, consequently, in death of bacillus. In addition, studies have demonstrated the influence of MICA genes in the pathogenesis of leprosy. Specifically, they may play a role in the interaction between NK cells and infected cells. Finally, pro- and anti-inflammatory cytokines have been influencing the clinical course of leprosy. Data from a wide variety of sources support the existence of genetic factors influencing the leprosy pathogenesis. These sources include twin studies, segregation analyses, family-based linkage and association studies, candidate gene association studies, and, most recently, genome-wide association studies (GWAS). The purpose of this brief review was to highlight the importance of some immune response genes and their correlation with the clinical forms of leprosy, as well as their implications for disease resistance and susceptibility.

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Leprosy in a high‐prevalence Egyptian village: epidemiology and risk factors

Cited by 25 publications

References 13 publications

HLA-DR and HLA-DQ alleles in patients from the south of Brazil: markers for leprosy susceptibility and resistance

HLA-DR and HLA-DQ alleles in patients from the south of Brazil: markers for leprosy susceptibility and resistance

ANCA patients have T cells responsive to complementary PR-3 antigen

Role ofHLA,KIR,MICA, and Cytokines Genes in Leprosy

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