| Yazarlar |
Dr. Öğr. Üyesi Güneş DİNÇ AKBULUT
Ahi Evran Üniversitesi, Türkiye |
Didem Özkazanç
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Güneş Esendağlı
Hacettepe Üniversitesi, Türkiye |
| Özet |
| The immune system is not only evolved to protect the body from pathogens, but it also recognizes and eliminates cancer cells. CD4+ helper T (Th) lymphocytes are central intercessors differentiated according to the character of physiological or pathological status. Generation of type 1 Th (Th1) cells is primarily associated with a pathological insult that must be removed through immune elimination. Upon interacting with other immune and transformed cells, Th1 cells can hamper cancer progression. Therefore, it is a major obstacle for tumor cells to become insensitive or resistant to Th1-oriented actions. The organism employs various mechanisms to return to a steady state and ensure tissue repair following a destructive inflammatory response. Th1 cells are also tightly regulated during the termination of immune responses. They can reduce the production of inflammatory cytokines, both generate and be prone to inhibitory signals, and undergo activation-induced cell death for inflammation resolution. Additionally, Th1 cells may become hyporesponsive, exhausted, and decorated with many inhibitory receptors and eventually lose functionality. There is growing evidence about tumor cells taking advantage of the strategies used for the resolution of Th1-oriented inflammation. Here, the current insights on Th1 cells during cancer-associated inflammatory responses are reviewed. |
| Anahtar Kelimeler |
| Makale Türü | Diğer (Teknik, not, yorum, vaka takdimi, editöre mektup, özet, kitap krıtiği, araştırma notu, bilirkişi raporu ve benzeri) |
| Makale Alt Türü | SCI, SSCI, AHCI, SCI-Exp dergilerinde yayımlanan teknik not, editöre mektup, tartışma, vaka takdimi ve özet türünden makale |
| Dergi Adı | TURKISH JOURNAL OF BIOLOGY |
| Dergi ISSN | 1300-0152 |
| Dergi Tarandığı Indeksler | SCI-Expanded |
| Makale Dili | İngilizce |
| Basım Tarihi | 02-2017 |
| Cilt No | 41 |
| Sayfalar | 20 / 30 |
| Doi Numarası | 10.3906/biy-1602-20 |
| Makale Linki | http://online.journals.tubitak.gov.tr/openDoiPdf.htm?mKodu=biy-1602-20 |
| Atıf Sayıları |
