1988
DOI: 10.1016/0092-8674(88)90486-2
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A novel form of TNF/cachectin is a cell surface cytotoxic transmembrane protein: Ramifications for the complex physiology of TNF

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Cited by 993 publications
(493 citation statements)
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“…The immunologic importance of the cell-associated cytokines is largely unknown. On the other hand, IL-1, 23 TNF, 24 LT␣ 25 and IFN␥ 26 are expressed in two different versions, one is a membrane-bound form and the other is soluble form. While precise functional discrimination of the forms has not been made, the membrane-bound form of TNF has a unique function distinct from that of the soluble TNF.…”
Section: Figure 3 Proliferation Of T Cell Clones In Response Tomentioning
confidence: 99%
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“…The immunologic importance of the cell-associated cytokines is largely unknown. On the other hand, IL-1, 23 TNF, 24 LT␣ 25 and IFN␥ 26 are expressed in two different versions, one is a membrane-bound form and the other is soluble form. While precise functional discrimination of the forms has not been made, the membrane-bound form of TNF has a unique function distinct from that of the soluble TNF.…”
Section: Figure 3 Proliferation Of T Cell Clones In Response Tomentioning
confidence: 99%
“…Several cytokines are expressed as membrane-associated forms, soluble forms or proteolytically processed forms; IL-1, 23 TNF, 24 LT␣, 25 and IFN␥. 26 Genetically engineered membrane-bound forms can result in lower tox- icity of TNF and LT␣.…”
Section: Introductionmentioning
confidence: 99%
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“…However, TNF-␣ is known to be produced as a membrane bound precursor, which requires proteolytic activation. 43 In order to find out whether TNF-␣ is released from NB4 cells, we determined soluble TNF-␣ in NB4 conditioned medium, which is a prequisite for the autocrine regulation we describe here.…”
Section: Figurementioning
confidence: 99%
“…IL-4 modulates IgE levels, resulting in inflammatory cell migration to inter-respiratory cells [8], and IL-13 induces morphological changes in the pulmonary system typical of asthma, such as mucous hypersecretion, epithelial hyperplasia, base membrane thickening, inflammatory cell infiltration, and B cell activation [912]. TNF-α is produced by macrophages and is involved in the interaction between mast cells [13] and airway smooth muscle cells, a key mechanism for inducing airway hyperresponsiveness [14]. In asthma, IL-6 is upregulated in pulmonary epithelial cells by various stimuli [15] and is involved in facilitating IL-4 differentiation, downregulating Th2 cell differentiation, and promoting Th17 cell differentiation [16].…”
Section: Introductionmentioning
confidence: 99%