期刊
JCI INSIGHT
卷 2, 期 19, 页码 -出版社
AMER SOC CLINICAL INVESTIGATION INC
DOI: 10.1172/jci.insight.95367
关键词
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资金
- Biological Resource Center Ferdinand Cabanne (Dijon, France) [BB-0033-00044]
- Institut National du Cancer (INCa) [2010-088]
- Comites Departementaux of Loire-Atlantique, Maine et Loire, Vendee and Finistere from the Ligue Nationale contre le Cancer
- Canceropole Grand Ouest
- NIH [P50GM085273]
- Gillson-Longenbaugh Foundation
- UNM Cancer Center Support Grant [P30 CA118100]
- Academic Science Education and Research Training-Institutional Research and Academic Career Development Award (ASERT IRACDA) [K12 GM088021]
- Region Pays de la Loire
- Region Centre
- INCa
Subsets of mature B cell neoplasms are linked to infection with intracellular pathogens such as Epstein-Barr virus (EBV), hepatitis C virus (HCV), or Helicobacter pylori. However, the association between infection and the immunoglobulin-secreting (Ig-secreting) B proliferative disorders remains largely unresolved. We investigated whether the monoclonal IgG (mc IgG) produced by patients diagnosed with monoclonal gammopathy of undetermined significance (MGUS) or multiple myeloma (MM) targets infectious pathogens. Antigen specificity of purified mc IgG from a large patient cohort (n = 244) was determined using a multiplex infectious-antigen array (MIAA), which screens for reactivity to purified antigens or lysates from 9 pathogens. Purified mc IgG from 23.4% of patients (57 of 244) specifically recognized 1 pathogen in the MIAA. EBV was the most frequent target (15.6%), with 36 of 38 mc IgGs recognizing EBV nuclear antigen-1 (EBNA-1). MM patients with EBNA-1-specific mc IgG (14.0%) showed substantially greater bone marrow plasma cell infiltration and higher beta(2)-microglobulin and inflammation/infection-linked cytokine levels compared with other smoldering myeloma/MM patients. Five other pathogens were the targets of mc IgG: herpes virus simplex-1 (2.9%), varicella zoster virus (1.6%), cytomegalovirus (0.8%), hepatitis C virus (1.2%), and H. pylori (1.2%). We conclude that a dysregulated immune response to infection may underlie disease onset and/or progression of MGUS and MM for subsets of patients.
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