Lymphotoxin, tumor necrosis factor, and gamma interferon are cytostatic for normal human keratinocytes.

Lymphotoxin, tumor necrosis factor, and gamma interferon are cytostatic for normal human keratinocytes.
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淋巴毒素、肿瘤坏死因子和γ干扰素对正常人角质形成细胞具有细胞抑制作用。

DOI:
10.1111/1523-1747.ep12696816
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发表时间:
1989
期刊:
The Journal of investigative dermatology
影响因子:
--
通讯作者:
Symington,FW
Symington,FW
中科院分区:
--
文献类型:
--
作者:
Symington,FW

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The effects of crude lymphokine-enriched supernatants, purified recombinant lymphotoxin (LT), tumor necrosis factor-α (TNF), and gamma interferon (γ IF) on proliferating human keratinocytes were assessed using two in vitro culture systems. Activated splenocyte supernatants inhibited keratinocyte colony growth on fibroblast feeder layers and arrested basal keratinocyte DNA synthesis within 24 h. Purified recombinant LT, TNF, and γ IF inhibited cell proliferation in serum-free medium without noticeably affecting viability. Cytostasis was dose-dependent (up to 90% with LT or TNF and 99% with γ IF) and was maximal within 24–36 h. Specific antibodies neutralized TNF- and γ IF-me- dilated cytostasis. Combined treatment with LT (or TNF) and γ IF increased the degree of cytostasis, particularly at low lymphokine concentrations. Maximum inhibition of DNA synthesis and the duration of exposure required for this inhibition were comparable for LT and TNF and differed for γ IF. Each of these lymphokines induced cell enlargement, flattening, and vesiculation, with γ IF alone or γ IF plus either LT or TNF. Flow cytometric studies of lymphokine-treated keratinocytes indicated that LT, TNF, and γ IF could enhance beta-2 microglobulin expression 1.5-fold to threefold, wheareas only γ IF induced class II antigens. Staining for class II and beta-2 microglobulin was reduced on cells treated with high concentrations of γ IF compared with either optimally treated or untreated cells. The potential relevance of these findings to cutaneous immune defense and disease is discussed.
DOI: --
发表时间: 1988
期刊: Journal of immunology (Baltimore, Md. : 1950)
影响因子: --
作者:
Koller,BH;Geraghty,DE;Shimizu,Y;DeMars,R;Orr,HT
通讯作者: Orr,HT
人类角质形成细胞在疾病中生物合成 HLA-DR 抗原的证据。
DOI: 10.1084/jem.159.6.1784
发表时间: 1984-06-01
期刊: The Journal of experimental medicine
影响因子: --
作者:
Volc-Platzer B;Majdic O;Knapp W;Wolff K;Hinterberger W;Lechner K;Stingl G
通讯作者: Stingl G
T 细胞杂交瘤产生淋巴毒素和肿瘤坏死因子。
DOI: 10.1016/s0021-9258(19)57227-1
发表时间: 1987
期刊: Immunology
影响因子: 6.4
作者:
Y. Kobayashi;M. Asada;T. Osawa
通讯作者: T. Osawa
源自人 T 细胞杂交瘤的人淋巴毒素 mRNA 的克隆和表达。
DOI: 10.1093/oxfordjournals.jbchem.a121765
发表时间: 1986
影响因子: 2.7
作者:
Y. Kobayashi;D. Miyamoto;M. Asada;M. Obinata;T. Osawa
通讯作者: T. Osawa
白细胞介素1和肿瘤坏死因子的协同抗增殖活性。
DOI: --
发表时间: 1987
期刊: Journal of immunology (Baltimore, Md. : 1950)
影响因子: --
作者:
Ruggiero,V;Baglioni,C
通讯作者: Baglioni,C