LILRA6 copy number variation correlates with susceptibility to atopic dermatitis

Leukocyte immunoglobulin-like receptors (LILR) are expressed mostly on myelomonocytic cells where they are mediators of immunological tolerance. Two LILR genes, LILRA3 and LILRA6, exhibit marked copy number variation. We assessed the contribution of these genes to atopic dermatitis (AD) by analysing...

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Autores principales: López-Álvarez, M. R., Jiang, W., Jones, D. C., Jayaraman, J., Johnson, C ., Cookson, W. O., Moffatt, M. F., Trowsdale, J., Traherne, J. A.
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Springer Berlin Heidelberg 2016
Materias:
Short Communication
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5026711/
https://www.ncbi.nlm.nih.gov/pubmed/27333811
http://dx.doi.org/10.1007/s00251-016-0924-z
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author López-Álvarez, M. R.
Jiang, W.
Jones, D. C.
Jayaraman, J.
Johnson, C .
Cookson, W. O.
Moffatt, M. F.
Trowsdale, J.
Traherne, J. A.
author_facet López-Álvarez, M. R.
Jiang, W.
Jones, D. C.
Jayaraman, J.
Johnson, C .
Cookson, W. O.
Moffatt, M. F.
Trowsdale, J.
Traherne, J. A.
author_sort López-Álvarez, M. R.
collection PubMed
description Leukocyte immunoglobulin-like receptors (LILR) are expressed mostly on myelomonocytic cells where they are mediators of immunological tolerance. Two LILR genes, LILRA3 and LILRA6, exhibit marked copy number variation. We assessed the contribution of these genes to atopic dermatitis (AD) by analysing transmission in 378 AD families. The data indicated that copies of LILRA6 were over-transmitted to affected patients. They are consistent with a contribution of LILR genes to AD. They could affect the equilibrium between activating and inhibitory signals in the immune response.
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spelling pubmed-50267112016-10-07 LILRA6 copy number variation correlates with susceptibility to atopic dermatitis López-Álvarez, M. R. Jiang, W. Jones, D. C. Jayaraman, J. Johnson, C . Cookson, W. O. Moffatt, M. F. Trowsdale, J. Traherne, J. A. Immunogenetics Short Communication Leukocyte immunoglobulin-like receptors (LILR) are expressed mostly on myelomonocytic cells where they are mediators of immunological tolerance. Two LILR genes, LILRA3 and LILRA6, exhibit marked copy number variation. We assessed the contribution of these genes to atopic dermatitis (AD) by analysing transmission in 378 AD families. The data indicated that copies of LILRA6 were over-transmitted to affected patients. They are consistent with a contribution of LILR genes to AD. They could affect the equilibrium between activating and inhibitory signals in the immune response. Springer Berlin Heidelberg 2016-06-22 2016 /pmc/articles/PMC5026711/ /pubmed/27333811 http://dx.doi.org/10.1007/s00251-016-0924-z Text en © The Author(s) 2016 Open Access This article is distributed under the terms of the Creative Commons Attribution 4.0 International License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made.
spellingShingle Short Communication
López-Álvarez, M. R.
Jiang, W.
Jones, D. C.
Jayaraman, J.
Johnson, C .
Cookson, W. O.
Moffatt, M. F.
Trowsdale, J.
Traherne, J. A.
LILRA6 copy number variation correlates with susceptibility to atopic dermatitis
title LILRA6 copy number variation correlates with susceptibility to atopic dermatitis
title_full LILRA6 copy number variation correlates with susceptibility to atopic dermatitis
title_fullStr LILRA6 copy number variation correlates with susceptibility to atopic dermatitis
title_full_unstemmed LILRA6 copy number variation correlates with susceptibility to atopic dermatitis
title_short LILRA6 copy number variation correlates with susceptibility to atopic dermatitis
title_sort lilra6 copy number variation correlates with susceptibility to atopic dermatitis
topic Short Communication
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5026711/
https://www.ncbi.nlm.nih.gov/pubmed/27333811
http://dx.doi.org/10.1007/s00251-016-0924-z
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