Origin of B-Cell Neoplasms in Autoimmune Disease

Autoimmune diseases (ADs) are associated with a number of B-cell neoplasms but the associations are selective in regard to the type of neoplasm and the conferred risks are variable. So far no mechanistic bases for these differential associations have been demonstrated. We speculate that developmenta...

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Main Authors:	Hemminki, Kari, Liu, Xiangdong, Ji, Jianguang, Försti, Asta
Format:	Online
Language:	English
Published:	Public Library of Science 2016
Online Access:	https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4927111/

id	pubmed-4927111
recordtype	oai_dc
spelling	pubmed-49271112016-07-18 Origin of B-Cell Neoplasms in Autoimmune Disease Hemminki, Kari Liu, Xiangdong Ji, Jianguang Försti, Asta Research Article Autoimmune diseases (ADs) are associated with a number of B-cell neoplasms but the associations are selective in regard to the type of neoplasm and the conferred risks are variable. So far no mechanistic bases for these differential associations have been demonstrated. We speculate that developmental origin of B-cells might propose a mechanistic rationale for their carcinogenic response to autoimmune stimuli and tested the hypothesis on our previous studies on the risks of B-cell neoplasms after any of 33 ADs. We found that predominantly germinal center (GC)-derived B-cells showed multiple associations with ADs: diffuse large B cell lymphoma associated with 15 ADs, follicular lymphoma with 7 ADs and Hodgkin lymphoma with 11 ADs. Notably, these neoplasms shared significant associations with 5 ADs (immune thrombocytopenic purpura, polymyositis/dermatomyositis, rheumatoid arthritis, Sjogren syndrome and systemic lupus erythematosis). By contrast, primarily non-GC neoplasms, acute lymphocytic leukemia, chronic lymphocytic leukemia and myeloma associated with 2 ADs only and mantle cell lymphoma with 1 AD. None of the neoplasms shared associated ADs. These data may suggest that autoimmune stimulation critically interferes with the rapid cell division, somatic hypermutation, class switch recombination and immunological selection of maturing B-cell in the GC and delivers damage contributing to transformation. Public Library of Science 2016-06-29 /pmc/articles/PMC4927111/ /pubmed/27355450 http://dx.doi.org/10.1371/journal.pone.0158360 Text en © 2016 Hemminki et al http://creativecommons.org/licenses/by/4.0/ This is an open access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/4.0/) , which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
repository_type	Open Access Journal
institution_category	Foreign Institution
institution	US National Center for Biotechnology Information
building	NCBI PubMed
collection	Online Access
language	English
format	Online
author	Hemminki, Kari Liu, Xiangdong Ji, Jianguang Försti, Asta
spellingShingle	Hemminki, Kari Liu, Xiangdong Ji, Jianguang Försti, Asta Origin of B-Cell Neoplasms in Autoimmune Disease
author_facet	Hemminki, Kari Liu, Xiangdong Ji, Jianguang Försti, Asta
author_sort	Hemminki, Kari
title	Origin of B-Cell Neoplasms in Autoimmune Disease
title_short	Origin of B-Cell Neoplasms in Autoimmune Disease
title_full	Origin of B-Cell Neoplasms in Autoimmune Disease
title_fullStr	Origin of B-Cell Neoplasms in Autoimmune Disease
title_full_unstemmed	Origin of B-Cell Neoplasms in Autoimmune Disease
title_sort	origin of b-cell neoplasms in autoimmune disease
description	Autoimmune diseases (ADs) are associated with a number of B-cell neoplasms but the associations are selective in regard to the type of neoplasm and the conferred risks are variable. So far no mechanistic bases for these differential associations have been demonstrated. We speculate that developmental origin of B-cells might propose a mechanistic rationale for their carcinogenic response to autoimmune stimuli and tested the hypothesis on our previous studies on the risks of B-cell neoplasms after any of 33 ADs. We found that predominantly germinal center (GC)-derived B-cells showed multiple associations with ADs: diffuse large B cell lymphoma associated with 15 ADs, follicular lymphoma with 7 ADs and Hodgkin lymphoma with 11 ADs. Notably, these neoplasms shared significant associations with 5 ADs (immune thrombocytopenic purpura, polymyositis/dermatomyositis, rheumatoid arthritis, Sjogren syndrome and systemic lupus erythematosis). By contrast, primarily non-GC neoplasms, acute lymphocytic leukemia, chronic lymphocytic leukemia and myeloma associated with 2 ADs only and mantle cell lymphoma with 1 AD. None of the neoplasms shared associated ADs. These data may suggest that autoimmune stimulation critically interferes with the rapid cell division, somatic hypermutation, class switch recombination and immunological selection of maturing B-cell in the GC and delivers damage contributing to transformation.
publisher	Public Library of Science
publishDate	2016
url	https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4927111/
_version_	1613601762711699456

Origin of B-Cell Neoplasms in Autoimmune Disease

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