HLA Class I Polymorphisms Influencing Both Peptide Binding and KIR Interactions Are Associated with Remission among Children with Atopic Dermatitis: A Longitudinal Study.
HLA Class I Polymorphisms Influencing Both Peptide Binding and KIR Interactions Are Associated with Remission among Children with Atopic Dermatitis: A Longitudinal Study.
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DOI：
10.4049/jimmunol.2001252
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发表时间：
2021-05-01
期刊：
影响因子：
--
通讯作者：
Monos DS
中科院分区：
文献类型：
--
作者：
Margolis DJ;Mitra N;Kim BS;Duke JL;Berna RA;Hoffstad OJ;Wasserman JR;Ferriola DA;Mosbruger TL;Wubbenhorst BS;Nathanson KL;Monos DS
Atopic dermatitis (AD) is a disease of immune dysregulation and skin barrier dysfunction with a relapsing, remitting course and has been associated with several different genetic risk variants. Human leukocyte antigens (HLA) represent a highly variable set of genes that code for cell surface protein molecules involved in the antigen-specific immune response, including the regulation or functioning of T-cells, natural killer (NK) cells, and antigen presenting cells. The purpose of this study was to evaluate associations between HLA Class I polymorphisms and the progression of AD over time. We evaluated the associations of AD symptoms and HLA Class I polymorphisms based on high resolution two-field typing in a longitudinal cohort of children with AD (up to 10-years of follow-up). Seven hundred ninety-two children were evaluated every 6 months resulting in 12,752 AD evaluations. Using generalized estimating equations, B*44:02 was found to be associated with AD remission (1.83 [1.35, 2.47]; pcorr=0.0015). The HLA-B residues at position 116 (D-aspartate) and 80 (T-threonine) were associated with remission (1.42 [1.13, 1.76] p=0.003, pcorr= 0.028) and (1.45 [1.17, 1.80] p=0.0008, pcorr=0.0024) respectively. B80T is a killer-cell immunoglobulin-like receptor (KIR) site. Our findings reveal that two axes of immune response (T-cell and NK cell) may influence disease progression. Identifying binding pocket changes in addition to other factors (e.g. allergens) that increase the risk or severity of AD can improve our understanding of the immunologic mechanisms associated with AD and may lead to personalized therapies for improving patient care.
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影响因子：
2.6
作者：
Gough SC;Simmonds MJ
通讯作者：
Simmonds MJ
影响因子：
10.9
作者：
Margolis, David J.;Kim, Brian;Apter, Andrea J.;Gupta, Jayanta;Hoffstad, Ole;Papadopoulos, Maryte;Mitra, Nandita
通讯作者：
Mitra, Nandita
影响因子：
20.3
作者：
Ferrara, GB;Bacigalupo, A;Frumento, G
通讯作者：
Frumento, G
影响因子：
2.7
作者：
Margolis DJ;Mitra N;Kim B;Gupta J;Hoffstad OJ;Papadopoulos M;Wubbenhorst B;Nathanson KL;Duke JL;Monos DS;Kamoun M
通讯作者：
Kamoun M
影响因子：
17.1
作者：
Mack, Madison R.;Brestoff, Jonathan R.;Kim, Brian S.
通讯作者：
Kim, Brian S.