Association of Human Leucocyte Antigen (HLA) class II with systemic lupus erythematosis (SLE) patients from western India

Dedhia, Leenam; Pradhan, Vandana; Ghosh, Kanjaksha; Nadkar, Milind; Parekh, Sunil

doi:10.1016/j.mgene.2018.03.011

Cited by 5 publications

(6 citation statements)

References 13 publications

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“…We then performed HLA imputation for classical HLA-DQA1, HLA-DPA1 and HLA-DPB1 genes for allelic association analysis. In our analysis, we convincingly validated DQA1*01:02 as a potential universal susceptibility risk factor for SLE development, consistent with the findings from Hungarian, Mexican, Han Chinese, Tunisian and Indian populations 17 29 34 37 38. In addition, we also newly identified DPA1*02:02 as a susceptibility allele, while DPA1*01:03 was identified as a protective allele with modest risk magnitudes in the Malay patients with SLE.…”

Section: Discussionsupporting

confidence: 87%

“…HLA class II alleles have been repeatedly shown to display strong associations with SLE across the major histocompatibility complex region, particularly in the DRB1 and DQB1 loci. In the current study, we observed that HLA-DRB1*15 and DQB1*03 alleles were the most important susceptibility and protective variants for SLE in Malays and other ethnic groups,9 11 13–18 20 29–31 34–38 40–43 suggesting that the genetic effects of these alleles are generalised to multiple ethnic populations of Caucasian, African and Asian descent.…”

Section: Discussionmentioning

confidence: 51%

“…To determine the generalisability or universal HLA risk factors for SLE development across different ethnic populations worldwide, we compared the current findings with the published significant SLE-associated HLA alleles from different populations/ethnic groups (ie, Caucasians,9–12 29–35 African13 36 37 and Asians14–18 20 21 38–43). We restricted our selection of published SLE-associated HLA risk factors which were genotyped by molecular methods.…”

Section: Methodsmentioning

confidence: 99%

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Human leucocyte antigens profiling in Malay female patients with systemic lupus erythematosus: are we the same or different?

et al. 2022

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ObjectiveSLE is a heterogeneous autoimmune disease, in terms of clinical presentation, incidence and severity across diverse ethnic populations. We investigated the human leucocyte antigens (HLA) profile (ie, HLA-A, HLA-B and HLA-C, HLA-DRB1, HLA-DQA1, HLA-DQB1, HLA-DPA1 and HLA-DPB1) in Malaysian Malay female patients with SLE and determined the generalisability of the published HLA risk factors across different ethnic populations globally including Malaysia.MethodsOne hundred Malay female patients with SLE were recruited between January 2016 and October 2017 from a nephrology clinic. All patients were genotyped for HLA-A, HLA-B, HLA-C, HLA-DRB1, HLA-DQA1, HLA-DQB1, HLA-DPA1 and HLA-DPB1 alleles using PCR sequence-specific oligonucleotides method on Luminex platform. A total of 951 HLA genotyped population-based Malay control subjects was used for association testing by means of OR with 95% CIs.ResultsOur findings convincingly validated common associations between HLA−A*11 (OR=1.65, p=3.36×10−3, corrected P (Pc)=4.03×10−2) and DQB1*05:01 (OR=1.56, p=2.02×10−2, Pc=non−significant) and SLE susceptibility in the Malay population. In contrast, DQB1*03:01 (OR=0.51, p=4.06×10−4, Pc=6.50×10−3) were associated with decreased risk of SLE in Malay population. Additionally, we also detected novel associations of susceptibility HLA genes (ie, HLA-B*38:02, DPA1*02:02, DPB1*14:01) and protective HLA genes (ie, DPA1*01:03). When comparing the current data with data from previously published studies from Caucasian, African and Asian populations, DRB1*15 alleles, DQB1*03:01 and DQA1*01:02 were corroborated as universal susceptibility and protective genes.ConclusionsThis study reveals multiple HLA alleles associated with susceptibility and protection against risk of developing SLE in Malay female population with renal disorders. In addition, the published data from different ethnic populations together with our study further support the notion that the genetic effects from association with DRB1*15:01/02, DQB1*03:01 and DQA1*01:02 alleles are generalised to multiple ethnic populations of Caucasian, African and Asian descents.

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Section: Discussionsupporting

confidence: 87%

Section: Discussionmentioning

confidence: 51%

Section: Methodsmentioning

confidence: 99%

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Human leucocyte antigens profiling in Malay female patients with systemic lupus erythematosus: are we the same or different?

et al. 2022

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“…HLA DRB1*16:02 was previously linked to an elevated risk of various autoimmune diseases, including Grave's disease, SLE, Sjogren's syndrome, neuromyelitis optica, and relapsing polychondritis. These autoimmune disorders are predominantly mediated by mechanisms of autoantibody formation (Dedhia et al, 2018;Shu et al, 2019). Genetic susceptibility of HLA alleles could potentially contribute to the development of an environment conducive to autoimmune pathology, leading to the coexistence of multiple autoimmune conditions.…”

Section: Discussionmentioning

confidence: 99%

Neurological complexity in systemic lupus erythematosus: insights into autoimmune encephalitis

Liana Halim,

Novia Putri

2023

SMJ IDI Surabaya

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Background: Autoimmune encephalitis (AE) is an inflammatory syndrome characterized by autoantibodies targeting the central nervous system (CNS), leading to a wide range of neurological and psychiatric manifestations. Objective: This systematic review aims to investigate the coexistence of AE and systemic lupus erythematosus (SLE) to shed light on potential underlying mechanisms. Materials and Methods: Following PRISMA guidelines, a comprehensive search was conducted using Boolean logic in research databases i.e., PubMed, ProQuest, ScienceDirect, and Web of Science to identify relevant studies on AE, SLE, and their potential correlation. After the initial screening, exclusion, and quality assessment using the Joanna Briggs Institute Critical Appraisal Checklist, 14 studies were included for analysis. Among 18 patients, 88.9% were female whose an average age was 31.9 ± 12.7 years. Clinical presentations were varied, including cognitive impairment (66.67%), seizures (61.1%), altered mental status (50%), and movement disorders. Neuroimaging and neurophysiological findings consistently aligned with encephalitis, with MRI abnormalities observed in 94.4% of cases. Various autoantibodies were identified, including anti-NMDAR, anti-AMPA-R2, and anti-GluR antibodies. Conclusion: The identification of neuronal antibodies is crucial, particularly in scenarios involving both neuropsychiatric SLE (NPSLE) and encephalitis. This investigation aims to reveal etiological insights. The ongoing debate revolves around whether SLE-related encephalitis is associated with NPSLE through SLE antibodies or involves distinct antibodies. Further clinical research is essential to clarify the pathogenic role of autoantibody in SLE-linked AE.

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“…SLE association signals in the MHC region are primarily located in HLA-DRB1 in the MHC class II region or HLA-DRB1-associated long-range HLA gene haplotypes in several ancestral populations [ 36 , 37 , 38 ]. Genetic variation in these HLA genes is a contributor to the formation of autoantibodies and plays a role in tissue damage due to lupus [ 39 , 40 , 41 ].…”

Section: The Role Of Genetic Predisposition In the Pathogenesis Of Slementioning

confidence: 99%

Disentangling the Pathogenesis of Systemic Lupus Erythematosus: Close Ties between Immunological, Genetic and Environmental Factors

Sutanto

Yuliasih

2023

Medicina

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Systemic Lupus Erythematosus (SLE) is a systemic autoimmune disease that attacks various organ systems with a variety of clinical implications, ranging from mild skin and mucosal manifestations to severe central nervous system manifestations and death. Cases of SLE have been documented nearly two centuries ago when scholars used the terms ‘erythema centrifugum’ and ‘seborrhea congestiva’ to describe the discoid skin lesions and the butterfly or malar rash in SLE. Since then, knowledge about this disease has developed rapidly, especially knowledge related to the underlying pathogenesis of SLE. To date, it is known that immune system dysregulation, supported by genetic and environmental predisposition, can trigger the occurrence of SLE in a group of susceptible individuals. Various inflammatory mediators, cytokines and chemokines, as well as intra- and intercellular signaling pathways, are involved in the pathogenesis of SLE. In this review, we will discuss the molecular and cellular aspects of SLE pathogenesis, with a focus on how the immune system, genetics and the environment interact and trigger the various clinical manifestations of SLE.

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Association of Human Leucocyte Antigen (HLA) class II with systemic lupus erythematosis (SLE) patients from western India

Cited by 5 publications

References 13 publications

Human leucocyte antigens profiling in Malay female patients with systemic lupus erythematosus: are we the same or different?

Human leucocyte antigens profiling in Malay female patients with systemic lupus erythematosus: are we the same or different?

Neurological complexity in systemic lupus erythematosus: insights into autoimmune encephalitis

Disentangling the Pathogenesis of Systemic Lupus Erythematosus: Close Ties between Immunological, Genetic and Environmental Factors

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