N-linked glycan modification on antigen-presenting cells restores an allospecific cytotoxic T cell response
نویسندگان
چکیده
The B6 anti-bm6 allospecific CTL response is strictly dependent on CD4+ cells when using LPS blasts as stimulator cells. Altering the N-linked carbohydrates on stimulator cells by use of the N-linked trimming glycosidase inhibitors 1-deoxymannojirimycin and swainsonine, or by treatment with bacterial neuraminidase, results in a restoration of the B6 anti-bm6 response in the absence of CD4+ cells. The extent of restoration is inversely correlated with the number of sialic acids present on N-linked glycans of stimulator cells.
منابع مشابه
Mgat2 ablation in the myeloid lineage leads to defective glycoantigen T cell responses.
N-linked glycosylation is a central regulatory factor that influences the immune system in varied and profound ways, including leukocyte homing, T cell receptor signaling and others. Moreover, N-glycan branching has been demonstrated to change as a function of infection and inflammation. Our previous findings suggest that complex-type N-glycans on the class II major histocompatibility complex p...
متن کاملGlycosylation of native MHC class Ia molecules is required for recognition by allogeneic cytotoxic T lymphocytes.
The question whether or not target cell N-linked carbohydrate participates in cytotoxic T lymphocyte (CTL) mediated cytolysis has been in contention for well over a decade. Much of the evidence supporting a role for N-linked carbohydrate stems from the treatment of target cells with the glycosylation inhibitor tunicamycin (TM). In this report, we show that treatment of targets with TM, but not ...
متن کاملتاثیر واکسن سلولهای دندریتیک فعال شده با اجزاء پروتیینی توکسوپلاسما گوندی بر سلولهای T از نوع CD8+ اختصاصی تومور
Normal 0 false false false EN-US X-NONE AR-SA MicrosoftInternetExplorer4 /* Style Definitions */ table.MsoNormalTable {mso-style-name:"Table Normal" mso-tsty...
متن کاملDeficiency of C5aR prolongs renal allograft survival.
Interaction between C5a, a product of complement activation, and its receptor (C5aR) upregulates antigen-specific T cell responses by modulating the activation of antigen-presenting cells and T cells. Whether this C5a-C5aR interaction contributes to the immune responses that promote renal allograft rejection is unknown. Here, we found that deficiency of C5aR in both graft and recipient reduced ...
متن کاملذخیره در منابع من
با ذخیره ی این منبع در منابع من، دسترسی به آن را برای استفاده های بعدی آسان تر کنید
برای دانلود متن کامل این مقاله و بیش از 32 میلیون مقاله دیگر ابتدا ثبت نام کنید
ثبت ناماگر عضو سایت هستید لطفا وارد حساب کاربری خود شوید
ورودعنوان ژورنال:
- The Journal of Experimental Medicine
دوره 171 شماره
صفحات -
تاریخ انتشار 1990