کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
10899516 | 1084383 | 2015 | 7 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
High-dose cyclophosphamide induces specific tumor immunity with concomitant recruitment of LAMP1/CD107a-expressing CD4-positive T cells into tumor sites
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کلمات کلیدی
FCMDLNcytolytic T cellHprtCFSETregsCTXAPCGAPDHMFIFITCCC chemokine - CC کیموکینCD4+ T cell - CD4 + T سلولCTLs - CTL هاHCC - HCCallophycocyanin - آلوفوکسیانینRegulatory T cells - سلولهای تی تنظیمکنندهCyclophosphamide - سیکلوفسفامید fluorescein isothiocyanate - فلوئورسین ایسوتیوسیاناتFlow cytometry - فلوسیتومتریcytolytic T lymphocytes - لنفوسیت های تی سیتولیتیکmean fluorescence intensity - میانگین شدت فلورسانسhypoxanthine phosphoribosyltransferase - هیپوکسانتین فسفریبوسیل ترانسفرازHepatocellular carcinoma - کارسینوم هپاتوسلولار(کارسینوم سلولهای استخوانی)Draining lymph node - گره لنفاوی تخلیهglyceraldehyde-3-phosphate dehydrogenase - گلیسرالیدید-3-فسفات دهیدروژناز
موضوعات مرتبط
علوم زیستی و بیوفناوری
بیوشیمی، ژنتیک و زیست شناسی مولکولی
تحقیقات سرطان
پیش نمایش صفحه اول مقاله
![عکس صفحه اول مقاله: High-dose cyclophosphamide induces specific tumor immunity with concomitant recruitment of LAMP1/CD107a-expressing CD4-positive T cells into tumor sites High-dose cyclophosphamide induces specific tumor immunity with concomitant recruitment of LAMP1/CD107a-expressing CD4-positive T cells into tumor sites](/preview/png/10899516.png)
چکیده انگلیسی
Cancer chemotherapy regimens, particularly those employing high-dose cytotoxic drugs such as cyclophosphamide (CTX), have been considered to be immune suppressive. However, we observed that a single administration of high-dose CTX abolished tumors arising from subcutaneous injection of a mouse hepatoma cell line and subsequently induced specific tumor immunity. Depletion of T cells, specifically CD4+ T cells, abrogated the CTX-mediated tumor regression. CTX treatment induced the rapid recruitment of CD4+ T cells into the tumors, and these recruited cells initiated expression of LAMP1/CD107a, a cytotoxic granule molecule, and granzyme B in the absence of antigen presentation at draining lymph nodes and proliferation in the tumor tissues. Moreover, CTX enhanced the expression of a CC chemokine, CCL3, in tumor tissues, and CTX-mediated tumor regression was attenuated in mice deficient in CCR5, the receptor for this chemokine. Consistently, less CTX-induced accumulation of intratumoral LAMP1/CD107a-expressing CD4+ T cells was observed in mice receiving splenocytes derived from CCR5-deficient mice than in those receiving splenocytes derived from WT mice. Thus, CTX induces the expression of CCL3, which induces the intratumoral migration of CD4+ T cells expressing cytotoxic molecules, leading to tumor eradication and subsequent specific tumor immunity.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Cancer Letters - Volume 366, Issue 1, 28 September 2015, Pages 93-99
Journal: Cancer Letters - Volume 366, Issue 1, 28 September 2015, Pages 93-99
نویسندگان
Tatsushi Naito, Tomohisa Baba, Kazuyoshi Takeda, Soichiro Sasaki, Yasunari Nakamoto, Naofumi Mukaida,