English (United Kingdom)

https://curated-unify.zendy.io/wp-json/zendy-region/v1/featured_content/oa?rat=en

https://curated-unify.zendy.io/wp-json/zendy-region/v1/highlighted_journal/

Global: Zendy Plus annual

Presents the access of premium content as premium feature

Premium Content

Presents the keyphrase highlighting as premium feature

Keyphrase Highlighting

Presents the summarisation as premium feature

Summarisation

Insights

Presents the pdf analysis as premium feature

PDF Analysis

Presents the zaia usage as premium feature

ZAIA

Global: Zendy Tools annual

Global: Zendy Free Plan

Global: Zendy Tools monthly

Global: Zendy Plus monthly

Non Hodgkin Lymphomas (NHL) complicating Hepatitis C virus (HCV) and Sjögren’s Syndrome (SS) share common characteristics. Genetic impairment of TNFAIP3/A20 contributes to lymphomagenesis in SS. We have studied genetic variants of TNFAIP3 in HCV patients with (n=87) and without (n=171) NHL. The prevalence of the rs2230926G variant did not differ between patients with and without NHL (p=0.51). However, among NHL patients, the rs2230926G allele was restricted to rheumatoid factor positive (RF+) patients (14.6% versus 0% in RFpatients, p=0.015). HCV infection is a new example of chronic antigenic stimulation where a coding variant of TNFAIP3 favor the lymphomatous escape of autoimmune B cells.

A Missense Variant of TNFAIP3 is Associated with the Presence of Rheumatoid Factor in Patients with HCV-Related Lymphoma