Heat shock enhances the expression of cytotoxic granule proteins and augments the activities of tumor-associated antigen-specific cytotoxic T lymphocytes View Full Text


Ontology type: schema:ScholarlyArticle      Open Access: True


Article Info

DATE

2012-07-11

AUTHORS

Akari Takahashi, Toshihiko Torigoe, Yasuaki Tamura, Takayuki Kanaseki, Tomohide Tsukahara, Yasushi Sasaki, Hidekazu Kameshima, Tetsuhiro Tsuruma, Koichi Hirata, Takashi Tokino, Yoshihiko Hirohashi, Noriyuki Sato

ABSTRACT

Focal inflammation causes systemic fever. Cancer hyperthermia therapy results in shrinkage of tumors by various mechanisms, including induction of adaptive immune response. However, the physiological meaning of systemic fever and mechanisms of tumor shrinkage by hyperthermia have not been completely understood. In this study, we investigated how heat shock influences the adaptive immune system. We established a cytotoxic T lymphocyte (CTL) clone (#IM29) specific for survivin, one of the tumor-associated antigens (TAAs), from survivin peptide-immunized cancer patients’ peripheral blood, and the CTL activities were investigated in several temperature conditions (37–41 °C). Cytotoxicity and IFN-γ secretion of CTL were greatest under 39 °C condition, whereas they were minimum under 41 °C. To address the molecular mechanisms of this phenomenon, we investigated the apoptosis status of CTLs, expression of CD3, CD8, and TCRαβ by flow cytometry, and expression of perforin, granzyme B, and Fas ligand by western blot analysis. The expression of perforin and granzyme B were upregulated under temperature conditions of 39 and 41 °C. On the other hand, CTL cell death was induced under 41 °C condition with highest Caspase-3 activity. Therefore, the greatest cytotoxicity activity at 39 °C might depend on upregulation of cytotoxic granule proteins including perforin and granzyme B. These results suggest that heat shock enhances effector phase of the adaptive immune system and promotes eradication of microbe and tumor cells. More... »

PAGES

757-763

References to SciGraph publications

Identifiers

URI

http://scigraph.springernature.com/pub.10.1007/s12192-012-0348-0

DOI

http://dx.doi.org/10.1007/s12192-012-0348-0

DIMENSIONS

https://app.dimensions.ai/details/publication/pub.1037633221

PUBMED

https://www.ncbi.nlm.nih.gov/pubmed/22777894


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25 schema:description Focal inflammation causes systemic fever. Cancer hyperthermia therapy results in shrinkage of tumors by various mechanisms, including induction of adaptive immune response. However, the physiological meaning of systemic fever and mechanisms of tumor shrinkage by hyperthermia have not been completely understood. In this study, we investigated how heat shock influences the adaptive immune system. We established a cytotoxic T lymphocyte (CTL) clone (#IM29) specific for survivin, one of the tumor-associated antigens (TAAs), from survivin peptide-immunized cancer patients’ peripheral blood, and the CTL activities were investigated in several temperature conditions (37–41 °C). Cytotoxicity and IFN-γ secretion of CTL were greatest under 39 °C condition, whereas they were minimum under 41 °C. To address the molecular mechanisms of this phenomenon, we investigated the apoptosis status of CTLs, expression of CD3, CD8, and TCRαβ by flow cytometry, and expression of perforin, granzyme B, and Fas ligand by western blot analysis. The expression of perforin and granzyme B were upregulated under temperature conditions of 39 and 41 °C. On the other hand, CTL cell death was induced under 41 °C condition with highest Caspase-3 activity. Therefore, the greatest cytotoxicity activity at 39 °C might depend on upregulation of cytotoxic granule proteins including perforin and granzyme B. These results suggest that heat shock enhances effector phase of the adaptive immune system and promotes eradication of microbe and tumor cells.
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32 C conditions
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37 FA
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39 T lymphocyte clones
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46 analysis
47 antigen
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49 apoptosis status
50 blood
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52 cancer hyperthermia therapy
53 cancer patients' peripheral blood
54 caspase-3 activity
55 cell death
56 cells
57 clones
58 conditions
59 cytometry
60 cytotoxic T lymphocyte clones
61 cytotoxic T lymphocytes
62 cytotoxic granule proteins
63 cytotoxicity
64 cytotoxicity activity
65 death
66 effector phase
67 eradication
68 eradication of microbes
69 expression
70 expression of CD3
71 expression of perforin
72 fever
73 flow cytometry
74 focal inflammation
75 granule proteins
76 granzyme B
77 granzyme B.
78 greater cytotoxicity activity
79 hand
80 heat shock
81 higher caspase-3 activity
82 hyperthermia
83 hyperthermia therapy
84 immune response
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95 patients' peripheral blood
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98 phase
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101 protein
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103 results
104 secretion
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107 shrinkage
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109 status
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111 survivin
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114 temperature conditions
115 therapy
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