Tumor Necrosis Factor/Cachectin Production by B-Cell Chronic Lymphocytic Leukemia and Hairy Cell Leukemia Cells

Foà, Robert; Massaia, Massimo; Tos, AG; Cardona, S; Guarini, Anna; Bianchi, Andrea; Attisano, C; Celle, Paola Francia di; Fierro, Mt

doi:10.1007/978-3-642-75510-1_30

Cited by 2 publications

(2 citation statements)

References 7 publications

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“…With regards to cancer development and progression, high doses of exogenous TNF-α induce death of tumour cells [44]. However, low concentrations of endogenous TNF-α promote tumour growth and spread [45]. Over the past 15 years the reports regarding the effects of TNF-α in angiogenesis have been contradictory and certainly intriguing.…”

Section: Tnfmentioning

confidence: 99%

Role of Inflammatory Mediators in Angiogenesis

Naldini

Carraro²

2005

CDTIA

264

187

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The angiogenic process involves several cell types and mediators, which interact to establish a specific microenvironment suitable for the formation of new capillaries from pre-existing vessels. Angiogenesis occurs in several physiological and pathological conditions, such as embryo development and wound healing, diabetic retinopathy and tumours. Inflammatory cells, namely monocytes/macrophages, T lymphocytes and neutrophils, fully participate in the angiogenic process by secreting cytokines that may affect endothelial cell (EC) functions, including EC proliferation, migration and activation. Angiogenesis is the result of a net balance between the activities exerted by positive and negative regulators. With regards to inflammatory cells and endothelium cross-talk, such balance is conceptually very similar to that of proinflammatory and anti-inflammatory mediators that modulate an appropriate inflammatory response. In this review we will mainly discuss the relevance of both physiological and pathological inflammatory processes in angiogenesis, with particular regards to microenvironmental contribution. We will also describe some of the most relevant pro-inflammatory cytokines in the modulation of the angiogenic process. Furthermore, we will concentrate on what has been recently reported about the mechanism by which some of these cytokines are induced during inflammation to promote a suitable microenvironment for angiogenesis and tumour progression. Pro-angiogenic cytokines, such as IL-1 and TNF, and anti-angiogenic cytokines such as IFN-γ and IL-12, will be briefly described. We will try to provide a rationale for the use of both cytokines and cytokine blockades as novel potential pharmaceutical targets to modulate angiogenesis in chronic inflammation as well as in cancer.

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Section: Tnfmentioning

confidence: 99%

Role of Inflammatory Mediators in Angiogenesis

Naldini

Carraro²

2005

CDTIA

264

187

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“…Moreover, elevated TNF-a levels have been observed in B-cell chronic lymphocytic leukemias (7), and T-cell membrane-bound TNF-a has been shown to be involved in human immunodeficiency virus (HIV)-induced polyclonal B-cell activation (8) and interleukin 4 (IL4)-induced immunoglobulin production (9).…”

mentioning

confidence: 99%

Tumor necrosis factor alpha is an autocrine growth factor for normal human B cells.

Boussiotis

Nadler

Strominger

et al. 1994

Proc. Natl. Acad. Sci. U.S.A.

140

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Transcription of the human tumor necrosis factor a (TNF-a) gene is one of the earliest events that occurs after stimulation of B or T cells via their antigen receptors. Antibody directed at surface immunoglobulin (anti-Ig) on B cells has previously been shown to induce a rapid burst of TNF-a gene transcription, which can be blocked by the immunosuppressants cyclosporin A (CsA) and FK506. Here, TNF-a gene transcription is shown also to be highly and rapidly induced in human B cells after stimulation via the CD40 and interleukin 4 pathways, which similarly is inhibited by CsA and a panel of CsA or FK506 analogues that block calcineurin phosphatase activity. Endogenous TNF-a produced after stimulation was involved in B-cell proliferation since anti-TNF-a monoclonal antibody inhibited both anti-Ig-and anti-CD40-induced B-cell proliferative responses. Moreover, addition of TNF-a during stimulation resulted in augmentation of B-cell proliferation, which was also inhibited by anti-TNF-a monoclonal antibody. Although lymphotoxin a (LT-a) mRNA is induced by both pathways, it is not blocked by CsA, whereas LT-I8nmRNA is constitutively expressed in B cells. Thus, TNF-a is a necessary autocrine growth factor for human B cells stimulated via two independent CsA-sensitive pathways and plays a role similar to that of interleukin 2 in T-cell proliferation. The autocrine nature of TNF-a in activated B cells implies a potential role for this cytokine in infection-related polyclonal B-cell expansion and in B-cell malignancies.

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Tumor Necrosis Factor/Cachectin Production by B-Cell Chronic Lymphocytic Leukemia and Hairy Cell Leukemia Cells

Cited by 2 publications

References 7 publications

Role of Inflammatory Mediators in Angiogenesis

Role of Inflammatory Mediators in Angiogenesis

Tumor necrosis factor alpha is an autocrine growth factor for normal human B cells.

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