A critical role for FcgammaRIIB in up-regulation of Fas ligand induced by a microbial polysaccharide

Piccioni, Miranda; Monari, Claudia; Bevilacqua, Sara; Perito, Stefano; Bistoni, Francesco; Kozel, Thomas R.; Vecchiarelli, Anna

doi:10.1111/j.1365-2249.2011.04415.x

Cited by 13 publications

(13 citation statements)

References 56 publications

(76 reference statements)

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“…Regarding the influence of GXM on APC function, it results in inhibition of T-cell proliferation [63]. Monocytes and macrophages, cell targets of GXM, show an alteration of costimulatory molecule expression and a prompt and long-lasting upregulation of the death receptor FasL, which in turn induces apoptosis of activated T cells via the FasL/Fas future science group Review Vecchiarelli, Pericolini, Gabrielli et al pathway [20,60]. Recently, the mechanism controlling FasL upregulation has been primarily ascribed to GXM/FcgRIIB interaction and it is mediated by activation of JNK, p38 and c-Jun [20].…”

Section: Future Science Groupmentioning

confidence: 98%

“…Monocytes and macrophages, cell targets of GXM, show an alteration of costimulatory molecule expression and a prompt and long-lasting upregulation of the death receptor FasL, which in turn induces apoptosis of activated T cells via the FasL/Fas future science group Review Vecchiarelli, Pericolini, Gabrielli et al pathway [20,60]. Recently, the mechanism controlling FasL upregulation has been primarily ascribed to GXM/FcgRIIB interaction and it is mediated by activation of JNK, p38 and c-Jun [20]. It is likely, therefore, that GXM can induce FasL upregulation by JNK and p38 activation following interaction with PRRs, particularly FcgRIIB (Figure 1, right side).…”

Section: Future Science Groupmentioning

confidence: 98%

“…TLR2 and TLR4 represent PRRs for glucuronoxylomannan (GXM); however, they seem to play a marginal role in the context of cryptococcal infection [19]. Indeed GXM induces marked inhibitory effects via binding to FcgRIIB [20] that counteract the activation occurring via TLR4, with consequent inhibition of the MAPK pathways necessary for proinflammatory cytokine release [19].…”

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confidence: 99%

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Elucidating the Immunological Function of the Cryptococcus Neoformans Capsule

et al. 2013

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The encapsulated fungal pathogen Cryptococcus neoformans represents a significant agent of life-threatening infections in immunocompromised subjects. A unique characteristic of Cryptococcus species is the presence of a polysaccharide capsule, which is essential for virulence and endows Cryptococcus with potent immunoregulatory properties. This review provides an overview of the immunological properties of the principal components of C. neoformans capsule.

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Section: Future Science Groupmentioning

confidence: 98%

Section: Future Science Groupmentioning

confidence: 98%

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confidence: 99%

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Elucidating the Immunological Function of the Cryptococcus Neoformans Capsule

et al. 2013

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“…In the brain, Glucuronoxylomannan, (GXM), the principal component of the cryptococcal polysaccharide capsule, binds to macrophage FcγRIIIB, which inhibits the Fcγ receptor and proinflammatory cytokine expression [29, 30], whereas mannoprotein induces antigen-specific T cell responses [31]. C. neoformans promotes an imbalance toward a Th2 response by suppressing T-helper (Th) 1 responses [32–34].…”

Section: Role Of Primary Immune or Host Responsementioning

confidence: 99%

The immunopathogenesis of cryptococcal immune reconstitution inflammatory syndrome

Meya

Manabe

Boulware³

et al. 2016

Current Opinion in Infectious Diseases

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Purpose of Review Cryptococcal meningitis (CM) causes significant mortality among HIV-infected patients, despite antifungal therapy and use of antiretroviral therapy (ART). In patients with CM, ART is often complicated by immune reconstitution inflammatory syndrome (IRIS), manifesting as unmasking of previously unrecognized subclinical infection (unmasking CM-IRIS) or paradoxical worsening of symptoms in the central nervous system after prior improvement with antifungal therapy (paradoxical CM-IRIS). We review our current understanding of the pathogenesis of this phenomenon, focusing on unifying innate and adaptive immune mechanisms leading to the development of this often fatal syndrome. Recent Findings We propose that HIV-associated CD4+ T cell depletion, chemokine-driven trafficking of monocytes into cerebrospinal fluid (CSF) in response to CM, and poor localized innate cytokine responses lead to inadequate cryptococcal killing and clearance of the fungus. Subsequent ART-associated recovery of T cell signaling and restored cytokine responses, characterized by Interferon-γ production, triggers an inflammatory response. The inflammatory response triggered by ART is dysregulated due to impaired homeostatic and regulatory mechanisms, culminating in the development of CM-IRIS. Summary Despite our incomplete understanding of the immunopathogenesis of CM-IRIS, emerging data exploring innate and adaptive immune responses could be exploited to predict, prevent and manage CM-IRIS and associated morbid consequences.

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“…The transient serum concentration could be even higher. Since the low affinity FcγRIIB receptor is highly expressed on the surface of B cells [34] and plays an important role in down-regulating immune responses [17,20,29,37], rituximab may directly target B cells by stimulating this receptor.…”

Section: Introductionmentioning

confidence: 99%

Rituximab inhibits Kv1.3 channels in human B lymphoma cells via activation of FcγRIIB receptors

Wang

et al. 2012

Biochimica et Biophysica Acta (BBA) - Molecular Cell Research

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Kv1.3 channels play an important role in modulating lymphocyte proliferation and apoptosis. We hypothesized that Kv1.3 channels in B lymphocytes might be regulated by rituximab, an antibody to CD20, a drug for treatments of B-cell lymphomas and autoimmune diseases. Using both whole-cell and cell-attached patch-clamp techniques, we found that rituximab inhibited Kv1.3 channels in Daudi human B lymphoma cells by promoting the channel inactivation at a concentration which was much greater than that required for activation of CD20. The effect of rituximab on Kv1.3 channels was abolished after selective blockade of FcγRIIB receptors with anti-FcγRIIB antibody. Western blot experiments showed that Daudi B cells expressed both Kv1.3 channel and the low affinity Fc receptor, FcγRIIB, which could be activated by the Fc region of rituximab. In contrast, normal lymphocytes expressed less Kv1.3 channels with faster inactivation. Confocal microscopy and flow cytometry data showed that rituximab induced apoptosis of Daudi B cells and that the effect was attenuated by blockade of FcγRIIB receptors and partially mimicked by inhibition of Kv1.3 channels. These results suggest that in addition to previously described complement-dependent cytotoxicity, rituximab also induces apoptosis of malignant B lymphocyte by stimulating FcγRIIB receptors and inhibiting Kv1.3 channels.

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A critical role for FcgammaRIIB in up-regulation of Fas ligand induced by a microbial polysaccharide

Cited by 13 publications

References 56 publications

Elucidating the Immunological Function of the Cryptococcus Neoformans Capsule

Elucidating the Immunological Function of the Cryptococcus Neoformans Capsule

The immunopathogenesis of cryptococcal immune reconstitution inflammatory syndrome

Rituximab inhibits Kv1.3 channels in human B lymphoma cells via activation of FcγRIIB receptors

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