Meta-analysis of the association between psoriasis and human leucocyte antigen-B

Zhao, Ya E; Ma, Jianxun; Li, Hu; Xiao, Shengxiang; Zhao, Yumei

doi:10.1111/bjd.12387

Cited by 9 publications

(7 citation statements)

References 57 publications

(350 reference statements)

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“…15 A recent meta-analysis demonstrated that HLA-B*37 and HLA-B*57 were strongly associated (OR > 3.0) with psoriasis. 31 The association of GT with HLA-B*58 is described for the first time in the present study. Marks and Tait (1980) found an increase in the frequency of B15 in patients with GT.…”

Section: Discussionsupporting

confidence: 59%

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A possible relationship of human leucocyte antigens with psoriasis vulgaris and geographic tongue

Picciani

Carneiro

Sampaio

et al. 2014

Acad Dermatol Venereol

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Section: Discussionsupporting

confidence: 59%

“…31 The association of GT with HLA-B*58 is described for the first time in the present study. Marks and Tait (1980) found an increase in the frequency of B15 in patients with GT.…”

supporting

confidence: 59%

A possible relationship of human leucocyte antigens with psoriasis vulgaris and geographic tongue

Picciani

Carneiro

Sampaio

et al. 2014

Acad Dermatol Venereol

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“…It has been confirmed that this allele is more common in patients with slow disease progression to AIDS, including elite HIV controllers [42]. HLA-B*5701 may also have a significant effect in diseases, such as psoriasis [46,47] and drug-related liver injury (DILI) [48]. HLAB5701 is currently the only genetic variant that is routinely and extensively tested in HIV-infected patients.…”

Section: Hla-b*5701mentioning

confidence: 99%

Genetic factors influencing HIV infection: a review

Aksak‐Wąs¹,

Parczewski²

2022

HIV & AIDS Review

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Patient's genetic background, especially in the HLA and CCR5 regions, strongly influences outcomes of HIV-1 infection. Understanding how host genetic factors can contribute to disease progression can help guide intervention strategies. To date, it has been estimated that HLA and CCR5 loci account for around 13% of variations in viremia set point. However, a key question in understanding all complex phenotypes, including HIV-1 progression, is what degree of influence different genetic variants can have.Presence of a 32bp deletion in CCR5 gene is associated with slower progression of HIV infection and positive effect on survival among cART untreated patients. Some studies have assessed CCR5-Δ32 as the most potent protective variant, both in immunological and viremic context, unrelated to HLA. Variants of CCR2 (rs1799864) are associated with slower progression to AIDS. CX3CR1 variant (rs3732378) may limit the shift in HIV-1 tropism from R5 to X4. This polymorphism may influence both disease progression and HIV tropism. HLA-C -35 (rs9264942) C/C variant is associated with a significant reduction in HIV viral load compared to T/T homozygote. Moreover, HLA-B*5701 has been confirmed to be more common in patients with slow disease progression to AIDS.Patient's genetic background, especially in HLA and CCR5 regions, strongly influences the progression of HIV-1 infection as well as viremic and immunologic values.

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“…HLA‐A*01:01 may act as a risk factor, participating in the pathological process of PsA in a Chinese Han population 13 . HLA‐B*38 , HLA‐B*13 , HLA‐B*37 , HLA‐B*27 , HLA‐B*17 and HLA‐Bw*16 are positively associated with PsA, while HLA‐B*12 and HLA‐Bw*35 are negatively associated with PsA in a White population 14 . As well as the HLA genes, the susceptibility non‐HLA genes are also shown as important in the pathogenesis of PsA.…”

Section: Introductionmentioning

confidence: 98%

Psoriatic arthritis: A systematic review of non‐HLA genetic studies and important signaling pathways

et al. 2020

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Psoriatic arthritis (PsA) is a chronic inflammatory disease that primarily invades the musculoskeletal system and skin. 1 Usually, besides the arthritis damage, including arthritis, enthesitis, dactylitis and axial involvement, patients with PsA have psoriatic skin, such as epidermal hyperplasia, hyperkeratosis, parakeratosis, Munro's microabscesses and mixed dermal infiltrates. 2 In general, the severity of a patient's joint symptoms is consistent with the severity of the skin lesions. 3 In some cases, patients with PsA without psoriatic skin features only have arthritis damage or finger pain, which is similar to rheumatoid arthritis (RA). Generally, only about 13% of patients with PsA have rheumatoid factor in the blood and synovial fluid, while more than 80% of RA patients can be detected with rheumatoid factor. 4 The prevalence of PsA around the world is 0.3%-1%, 4 which differs in race and regions. In Western countries, the prevalence rates are about 0.02%, 0.42% and 0.25% in Sweden, Italy and the USA respectively, 5,6 whereas the rates are relatively lower in the Eastern countries, ranging from 0.01% to 0.1% in China, and <0.00001% in Japan. 6 PsA is not only harmful to an individual's health and life quality, but also may lead to a higher risk to suffer from cardiovascular events. 7 The pathogenesis of PsA is complex, and itmay be caused by genetic and environmental factors. Environmental aspects include infections (eg infectious diarrhea, human immunodeficiency virus infection), smoking, trauma and obesity. 8-11 In the researches for susceptibility genes for PsA, some human leukocyte antigen (HLA) genes are found as risk factors, and some HLA genes are found as protect factors. For instances, HLA-B*38 and HLA-Cw6 alleles are

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Meta-analysis of the association between psoriasis and human leucocyte antigen-B

Abstract: A significant association was identified between psoriasis and 50 HLA-B alleles. The association varied in terms of race, and clinical type and onset age of psoriasis.

Cited by 9 publications

References 57 publications

A possible relationship of human leucocyte antigens with psoriasis vulgaris and geographic tongue

A possible relationship of human leucocyte antigens with psoriasis vulgaris and geographic tongue

Genetic factors influencing HIV infection: a review

Psoriatic arthritis: A systematic review of non‐HLA genetic studies and important signaling pathways

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