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/

Zendy Plus

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

Zendy Tools

Zendy Open

Immune escape and tolerance in the tumor microenvironment are closely involved in tumor progression, and are caused by T‐cell exhaustion and mediated by the inhibitory signaling of immune checkpoint molecules including programmed death‐1 ( PD ‐1), cytotoxic T‐lymphocyte associated protein 4, and T‐cell immunoglobulin and mucin domaincontaining molecule‐3. In the present study, we investigated the expression of the  PD ‐1 ligand 1 ( PD ‐L1) in a lymphoma microenvironment using paraffin‐embedded tissue samples, and subsequently studied the detailed mechanism of upregulation of  PD ‐L1 on macrophages using cultured human macrophages and lymphoma cell lines. We found that macrophages in lymphoma tissues of almost all cases of adult T‐cell leukemia/lymphoma ( ATLL ), follicular lymphoma and diffuse large B‐cell lymphoma expressed  PD ‐L1. Cell culture studies showed that the conditioned medium of  ATL ‐T and  SLVL  cell lines induced increased expression of  PD ‐L1/2 on macrophages, and that this  PD ‐L1/2 overexpression was dependent on activation of signal transducer and activator of transcription 3 (Stat3).  In vitro  studies including cytokine array analysis showed that  IL ‐27 (heterodimer of p28 and  EBI 3) induced overexpression of  PD ‐L1/2 on macrophages via Stat3 activation. Because lymphoma cell lines produced  IL ‐27B ( EBI 3) but not  IL ‐27p28, it was proposed that the  IL ‐27p28 derived from macrophages and the  IL ‐27B ( EBI 3) derived from lymphoma cells formed an  IL ‐27 (heterodimer) that induced  PD ‐L1/2 overexpression. Although the significance of  PD ‐L1/2 expressions on macrophages in lymphoma progression has never been clarified, an  IL ‐27‐Stat3 axis might be a target for immunotherapy for lymphoma patients.

An IL‐27/Stat3 axis induces expression of programmed cell death 1 ligands ( PD ‐L1/2) on infiltrating macrophages in lymphoma