ArticleClinical and experimental immunology2011
A critical role for FcgammaRIIB in up-regulation of Fas ligand induced by a microbial polysaccharide.
Article in Clinical and experimental immunology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed, 14 citations in OpenAlex.
- Review
- Cryptococcus neoformans Coinfection Dampens the TNF-α Response in HIV-1-Infected Human THP-1 Macrophages.mSphere · 2021Article
- Pentraxin-3 polymorphisms and pulmonary fungal disease in non-neutropenic patients.Annals of translational medicine · 2020Article
- Methamphetamine Impairs IgG1-Mediated Phagocytosis and Killing of Cryptococcus neoformans by J774.16 Macrophage- and NR-9640 Microglia-Like Cells.Infection and immunity · 2019Article
- Immunomodulatory Role of Capsular Polysaccharides Constituents ofFrontiers in medicine · 2019Review
- Involvement of the capsular GalXM-induced IL-17 cytokine in the control of Cryptococcus neoformans infection.Scientific reports · 2018Article
- Immune Recognition of Fungal Polysaccharides.Journal of fungi (Basel, Switzerland) · 2017Review
- The immunopathogenesis of cryptococcal immune reconstitution inflammatory syndrome: understanding a conundrum.Current opinion in infectious diseases · 2016Review
- Article
- Masking the Pathogen: Evolutionary Strategies of Fungi and Their Bacterial Counterparts.Journal of fungi (Basel, Switzerland) · 2015Review
- Capsular Material of Cryptococcus neoformans: Virulence and Much More.Mycopathologia · 2012Article
- Rituximab inhibits Kv1.3 channels in human B lymphoma cells via activation of FcγRIIB receptors.Biochimica et biophysica acta · 2012Article
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 2 countries.
Funding
Abstract
The microbial capsular polysaccharide glucuronoxylomannan (GXM) from the opportunistic fungus Cryptoccocus neoformans is able to alter the innate and adaptive immune response through multi-faceted mechanisms of immunosuppression. The ability of GXM to dampen the immune response involves the induction of T cell apoptosis, which is dependent on GXM-induced up-regulation of Fas ligand (FasL) on antigen-presenting cells. In this study we elucidate the mechanism exploited by GXM to induce up-regulation of FasL. We demonstrate that (i) the activation of FasL is dependent on GXM interaction with FcgammaRIIB (FcγRIIB); (ii) GXM induces activation of c-Jun NH(2) -terminal kinase (JNK) and p38 signal transduction pathways via FcγRIIB; (iii) this leads to downstream activation of c-Jun; (iv) JNK and p38 are simultaneously, but independently, activated; (v) FasL up-regulation occurs via JNK and p38 activation; and (vi) apoptosis occurs via FcγRIIB engagement with consequent JNK and p38 activation. Our results highlight a fast track to FasL up-regulation via FcγRIIB, and assign to this receptor a novel anti-inflammatory role that also accounts for induced peripheral tolerance. These results contribute to our understanding of the mechanism of immunosuppression that accompanies cryptococcosis.
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Registered trials
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