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The Suppressed Induction of Human Mature Cytotoxic T Lymphocytes Caused by Asbestos Is Not due to Interleukin-2 Insufficiency

We previously reported that exposure to chrysotile B (CB) asbestos suppressed the induction of mature cytotoxic T lymphocytes (CTLs) during mixed lymphocyte reaction assays (MLRs) with a decrease in the proliferation of immature CTLs. However, the mechanism responsible for the effect of asbestos fib...

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Published in:Journal of immunology research 2016-01, Vol.2016 (2016), p.1-10
Main Authors: Otsuki, Takemi, Yoshitome, Kei, Lee, Suni, Matsuzaki, Hidenori, Nishimura, Yasumitsu, Kumagai-Takei, Naoko, Hayashi, Hiroaki
Format: Article
Language:English
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Summary:We previously reported that exposure to chrysotile B (CB) asbestos suppressed the induction of mature cytotoxic T lymphocytes (CTLs) during mixed lymphocyte reaction assays (MLRs) with a decrease in the proliferation of immature CTLs. However, the mechanism responsible for the effect of asbestos fibers on the differentiation of CTLs remains unclear. Since interleukin-2 (IL-2) is a regulator of T lymphocyte proliferation, we examined the effect of IL-2 addition on suppressed CTL differentiation in CB-exposed cultures using flow cytometry (FCM). When IL-2 was added at 1 ng/mL on the second day of MLRs, the asbestos-caused decreases in the proliferation and percentages of CD25+ and CD45RO+ cells in CD8+ lymphocytes were not recovered by IL-2 addition, although the decrease in percentage of granzyme B+ cells was partially recovered. CD8+ lymphocytes from the IL-2-treated culture with asbestos showed the same degree of cytotoxicity as those in cultures without IL-2 or asbestos. These findings indicate that IL-2 insufficiency is not the main cause for the suppressed induction of CTLs by asbestos exposure, although they suggest a potential for the improvement of such suppressed CTL functions. Secretory factors other than IL-2 in addition to membrane-bound stimulatory molecules may play a role in asbestos-caused suppressed CTL differentiation.
ISSN:2314-8861
2314-7156
DOI:10.1155/2016/7484872