Cytokines as a link between innate and adaptive antitumor immunity

Belardelli, Filippo; Ferrantini, Maria

doi:10.1016/s1471-4906(02)02195-6

Cited by 279 publications

(164 citation statements)

References 60 publications

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“…Recent studies on the immunomodulatory activity of type I IFNs have shown that IFNs act on T-lymphocytes or dendritic cells to modulate their functions, which may explain IFN-induced tumor immunity (reviewed in Ref. 52). …”

Section: ) Dysregulation Of Weak Ifn-α α αmentioning

confidence: 99%

New aspects of IFN‐α/β signalling in immunity, oncogenesis and bone metabolism

Takaoka¹,

Taniguchi²

2003

Cancer Science

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Although interferons (IFNs) were originally identified as humoral factors that confer an antiviral state upon cells, they have been demonstrated to be multifunctional in a variety of biological systems. The IFN‐α/β system modulates not only the cellular immune response to viral and bacterial infections, but also the oncogenic process and bone metabolism. Further studies have revealed additional unique facets of the IFN‐α/β system. A weak signal by constitutively produced IFN‐α/β is critical not only for the regulation of cellular amplification of IFN‐α/β production upon viral infection or the enhancement of signalling by other cytokines, but also for the regulation of adaptive immune responses, such as the enhancement of CD8+ T cell activation. Furthermore, IFN‐β signalling is critical for the regulation of the bone‐resorbing osteo‐clasts. In this review, we focus on the newly discovered roles of the IFN‐α/β system in host defense and bone remodeling, particularly on the functions of the weak IFN‐α/β signalling in the context of what we refer to as the “rewing‐up” model. (Cancer Sci 2003; 94: 405–411)

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Section: ) Dysregulation Of Weak Ifn-α α αmentioning

confidence: 99%

New aspects of IFN‐α/β signalling in immunity, oncogenesis and bone metabolism

Takaoka¹,

Taniguchi²

2003

Cancer Science

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“…[14][15][16]. For example, IFN␣ is known to stimulate differentiation of functionally efficient monocyte-derived dendritic cells (17)(18)(19) and to promote survival and differentiation of activated T lymphocytes (20) and B lymphocytes (21,22).…”

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confidence: 99%

Induction of interferon‐α production in plasmacytoid dendritic cells by immune complexes containing nucleic acid released by necrotic or late apoptotic cells and lupus IgG

Lövgren

Eloranta

Båve

et al. 2004

Arthritis & Rheumatism

504

411

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Objective. To investigate the release of interferon-␣ (IFN␣)-inducing material by necrotic or apoptotic cells, its properties, and the necessity of autoantibodies from systemic lupus erythematosus (SLE) patients for the interferogenic activity.Methods. U937 monocytic leukemia cells or peripheral blood mononuclear cells (PBMCs) were rendered necrotic by freeze-thawing or apoptotic by treatment with ultraviolet light. Cell culture supernatants from these cells and IgG from SLE patients (SLE IgG) were added to cultures of normal PBMCs or purified plasmacytoid dendritic cells (PDCs). The importance of nucleic acids for IFN␣ induction was investigated by RNase and DNase treatment. The IFN␣ levels were measured by immunoassay.Results. Both necrotic and apoptotic U937 cells released material that, combined with SLE IgG, induced IFN␣ production in PDCs. The release from apoptotic cells occurred with a 16-hour delay, in late apoptosis. Also, normal PBMCs released IFN␣-inducing material, but only during necrosis. The interferogenic activity of the necrotic material required the presence of RNA, while both RNA and DNA were important in the apoptotic material. In both cases, the presence of SLE IgG was necessary, and its activity correlated with the presence of antibodies to RNA-binding proteins, but not anti-DNA antibodies.Conclusion. Necrotic and late apoptotic cells release material that, combined with SLE IgG, induces production of IFN␣ in PDCs. The IFN␣ inducers probably consist of immune complexes (ICs) containing RNA and possibly DNA as essential interferogenic components. The presence of such interferogenic ICs could explain the ongoing production of IFN␣ in SLE and could be of etiopathogenic importance.

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“…The interferon (IFN) family of cytokines regulates a number of physiological responses including innate defenses against viral, bacterial, and parasitic pathogens; the development of neoplastic growth; and specific immunity (6,21,28,31,74,78). IFN-induced activities are driven largely through an induction of cellular IFN-stimulated genes (ISGs).…”

mentioning

confidence: 99%