Abstract:
:A direct correlation between the constitutive expression of IL-1 alpha and reduced tumorigenicity of fibrosarcomas was observed. This was established in fibrosarcoma cell lines which produce IL-1 alpha 'spontaneously', possibly as an aberration of oncogene-mediated transformation or upon IL-1 alpha gene transfer. In fibroblasts intracellular or membrane-associated IL-1 alpha is expressed, whereas the secreted form of the cytokine (IL-1 beta) is absent. Studies on the mechanisms of tumor regression of the IL-1 alpha-positive fibroblastoid cell lines indicated that IL-1 alpha potentiates the development of tumor cell-specific CTLs, which are of importance for tumor eradication. Thus, IL-1 alpha induces enhanced helper T cell activity which provides auxiliary signals for the growth/development of CTLs. Non-adaptive effector cells, activated locally by IL-1 alpha-expressing fibrosarcoma cells, also contribute to the eradication of IL-1 alpha-expressing fibrosarcomas. Local IL-1 alpha expression potentiated antigen presentation, by the malignant fibroblasts as well as by tissue-resident antigen-presenting cells, thus further potentiating anti-tumor immune responses. Mice, in which IL-1 alpha-producing tumors were regressed, developed an immune memory and rejected a challenge with an IL-1 non-producing violent tumor cell line. Endogenous IL-1 alpha activates a cytokine cascade (i.e., IL-6, CSF), produced by the malignant cells and possibly also by stromal cells. However, IL-1 alpha expression is essential for fibrosarcoma eradication, while other cytokines possibly amplify and sustain its action.(ABSTRACT TRUNCATED AT 250 WORDS)
journal_name
Immunol Lettjournal_title
Immunology lettersauthors
Apte RN,Douvdevani A,Zoller M,White RM,Dvorkin T,Shimoni N,Fima E,Hacham M,Huleihel M,Benharroch Ddoi
10.1016/0165-2478(93)90163-vsubject
Has Abstract,Author List Incompletepub_date
1993-12-01 00:00:00pages
45-52issue
1eissn
0165-2478issn
1879-0542pii
0165-2478(93)90163-Vjournal_volume
39pub_type
杂志文章,评审abstract::Lck is the principal signal-generating tyrosine kinase of the T cell activation mechanism. We have previously demonstrated that induced Lck activation outside of lipid rafts (LR) results in the rapid translocation of a fraction of Lck to LR. While this translocation predicates the subsequent production of IL-2, the me...
journal_title:Immunology letters
pub_type: 杂志文章
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更新日期:2012-02-29 00:00:00
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journal_title:Immunology letters
pub_type: 杂志文章
doi:10.1016/0165-2478(96)02550-3
更新日期:1996-06-01 00:00:00
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journal_title:Immunology letters
pub_type: 杂志文章
doi:10.1016/s0165-2478(99)00123-6
更新日期:1999-10-01 00:00:00
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journal_title:Immunology letters
pub_type: 杂志文章
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更新日期:1994-12-01 00:00:00
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journal_title:Immunology letters
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journal_title:Immunology letters
pub_type: 杂志文章
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更新日期:2014-11-01 00:00:00
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journal_title:Immunology letters
pub_type: 杂志文章
doi:10.1016/j.imlet.2015.10.006
更新日期:2015-12-01 00:00:00
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journal_title:Immunology letters
pub_type: 杂志文章,评审
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更新日期:2014-07-01 00:00:00
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journal_title:Immunology letters
pub_type: 杂志文章
doi:10.1016/0165-2478(91)90150-9
更新日期:1991-03-01 00:00:00
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journal_title:Immunology letters
pub_type: 杂志文章
doi:10.1016/s0165-2478(99)00015-2
更新日期:1999-04-15 00:00:00
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journal_title:Immunology letters
pub_type: 杂志文章
doi:10.1016/s0165-2478(98)00077-7
更新日期:1998-11-01 00:00:00
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journal_title:Immunology letters
pub_type: 杂志文章
doi:10.1016/0165-2478(86)90102-1
更新日期:1986-03-01 00:00:00
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journal_title:Immunology letters
pub_type: 杂志文章
doi:10.1016/j.imlet.2020.12.011
更新日期:2021-02-01 00:00:00
abstract::Members of the transforming growth factor beta (TGF-beta) superfamily are soluble factors that regulate a variety of functional responses including proliferation, differentiation, apoptosis and cell cycle, among others, depending not only on the cell type and its differentiation state, but also on the milieu of cytoki...
journal_title:Immunology letters
pub_type: 杂志文章,评审
doi:10.1016/j.imlet.2006.12.010
更新日期:2007-03-15 00:00:00
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journal_title:Immunology letters
pub_type: 杂志文章
doi:10.1016/j.imlet.2016.04.008
更新日期:2016-06-01 00:00:00
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journal_title:Immunology letters
pub_type: 杂志文章
doi:10.1016/0165-2478(90)90184-r
更新日期:1990-10-01 00:00:00
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journal_title:Immunology letters
pub_type: 杂志文章
doi:10.1016/s0165-2478(97)00110-7
更新日期:1997-11-01 00:00:00
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journal_title:Immunology letters
pub_type: 杂志文章,评审
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更新日期:2003-01-22 00:00:00
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journal_title:Immunology letters
pub_type: 杂志文章
doi:10.1016/0165-2478(82)90084-0
更新日期:1982-07-01 00:00:00
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journal_title:Immunology letters
pub_type: 杂志文章,评审
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journal_title:Immunology letters
pub_type: 杂志文章
doi:10.1016/0165-2478(85)90178-6
更新日期:1985-01-01 00:00:00
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journal_title:Immunology letters
pub_type: 杂志文章
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journal_title:Immunology letters
pub_type: 杂志文章
doi:10.1016/s0165-2478(98)00060-1
更新日期:1998-10-01 00:00:00
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journal_title:Immunology letters
pub_type: 杂志文章
doi:10.1016/0165-2478(85)90004-5
更新日期:1985-01-01 00:00:00
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journal_title:Immunology letters
pub_type: 杂志文章
doi:10.1016/0165-2478(84)90037-3
更新日期:1984-01-01 00:00:00
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journal_title:Immunology letters
pub_type: 杂志文章,评审
doi:10.1016/s0165-2478(99)00024-3
更新日期:1999-05-03 00:00:00
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journal_title:Immunology letters
pub_type: 杂志文章
doi:10.1016/j.imlet.2018.03.012
更新日期:2018-06-01 00:00:00
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journal_title:Immunology letters
pub_type: 杂志文章
doi:10.1016/s0165-2478(03)00049-x
更新日期:2003-07-03 00:00:00
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journal_title:Immunology letters
pub_type: 杂志文章
doi:10.1016/0165-2478(89)90134-x
更新日期:1989-07-01 00:00:00
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journal_title:Immunology letters
pub_type: 杂志文章
doi:10.1016/0165-2478(87)90071-x
更新日期:1987-05-01 00:00:00