Academic Journal

ASC modulates CTL cytotoxicity and transplant outcome independent of the inflammasome

التفاصيل البيبلوغرافية
العنوان: ASC modulates CTL cytotoxicity and transplant outcome independent of the inflammasome
المؤلفون: Cheong, Melody, Gartlan, Kate H., Lee, Jason S., Tey, Siok-Keen, Zhang, Ping, Kuns, Rachel D., Andoniou, Christopher E., Martins, Jose Paulo, Chang, Karshing, Sutton, Vivien R., Kelly, Greg, Varelias, Antiopi, Vuckovic, Slavica, Markey, Kate A., Boyle, Glen M., Smyth, Mark J., Engwerda, Christian R., MacDonald, Kelli P.A., Trapani, Joseph A., Degli-Esposti, Mariapia A., Koyama, Motoko, Hill, Geoffrey R.
بيانات النشر: American Association for Cancer Research
سنة النشر: 2020
المجموعة: The University of Queensland: UQ eSpace
مصطلحات موضوعية: Immunology, Cancer Research, 1306 Cancer Research, 2403 Immunology
الوصف: The adaptor protein ASC (apoptosis-associated speck-like protein containing a CARD) is known to facilitate caspase-1 activation, which is essential for innate host immunity via the formation of the inflammasome complex, a multiprotein structure responsible for processing IL1β and IL18 into their active moieties. Here, we demonstrated that ASC-deficient CD8+ T cells failed to induce severe graft-versus-host disease (GVHD) and had impaired capacity for graft rejection and graft-versus-leukemia (GVL) activity. These effects were inflammasome-independent because GVHD lethality was not altered in recipients of caspase-1/11-deficient T cells. We also demonstrated that ASC deficiency resulted in a decrease in cytolytic function, with a reduction in granzyme B secretion and CD107a expression by CD8+ T cells. Altogether, our findings highlight that ASC represents an attractive therapeutic target for improving outcomes of clinical transplantation.
نوع الوثيقة: article in journal/newspaper
اللغة: English
تدمد: 2326-6066
2326-6074
Relation: orcid:0000-0002-0343-1274; orcid:0000-0001-9567-382X; 1078671 %7C 1173958; Not set
الاتاحة: https://espace.library.uq.edu.au/view/UQ:95b7dc9
رقم الانضمام: edsbas.6D3A7C23
قاعدة البيانات: BASE