scholarly journals Glycodendropeptides stimulate dendritic cell maturation and T cell proliferation: a potential influenza A virus immunotherapy

MedChemComm ◽  
2015 ◽  
Vol 6 (10) ◽  
pp. 1755-1760 ◽  
Author(s):  
Ainhoa Mascaraque ◽  
Wioleta Kowalczyk ◽  
Tahia Fernández ◽  
Francisca Palomares ◽  
Cristobalina Mayorga ◽  
...  

A GDP displaying the NP366–374 influenza A virus epitope induces an immunostimulatory effect, emerging as a potential flu vaccine.

2008 ◽  
Vol 180 (10) ◽  
pp. 6623-6628 ◽  
Author(s):  
Clinton S. Robbins ◽  
Francesca Franco ◽  
Majd Mouded ◽  
Manuela Cernadas ◽  
Steven D. Shapiro

2012 ◽  
Vol 64 (10) ◽  
pp. 3179-3188 ◽  
Author(s):  
Colt Egelston ◽  
Júlia Kurkó ◽  
Timea Besenyei ◽  
Beata Tryniszewska ◽  
Tibor A. Rauch ◽  
...  

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Kenjiro Kumano ◽  
Mazhar A. Kanak ◽  
Prathab Balaji Saravanan ◽  
J. P. Blanck ◽  
Yang Liu ◽  
...  

AbstractThe immunosuppressive regimen for clinical allogeneic islet transplantation uses beta cell–toxic compounds such as tacrolimus that cause islet graft loss. Previously we reported that the plant-derived steroidal lactone Withaferin A (WA) can protect islet grafts by inhibiting nuclear factor-kappa B (NF-κB). Since the NF-κB signaling pathway is essential for T-cell activation, we hypothesized that long-term WA administration may also provide an immunosuppressive effect. Treatment of BALB/c donor islets and C57BL/6N recipients with WA alone resulted in 80% islet graft long-term survival vs. 40% in low-dose FK506-treated mice. In vitro, WA significantly blocked mouse and human T-cell proliferation by CD3/CD28 bead stimulation and in mixed lymphocyte reaction assay. Treatment of immature dendritic cells with WA prevented their maturation in response to inflammatory stimuli, as seen by decreased expression of CD83 and human leukocyte antigen–DR isotype. Exosomes released by islets treated with WA contained significantly fewer proinflammatory molecules interleukin-6, interleukin-8, monocyte chemoattractant protein-1, interferon-gamma-induced protein-10, inducible nitric oxide synthase, and cyclooxygenase-2. In conclusion, WA treatment not only reduced inflammation but also prolonged allograft survival, possibly through suppression of dendritic cell maturation and T-cell proliferation. WA has the potential to inhibit both the innate and adaptive immune response to prolong allograft survival.


2010 ◽  
Vol 20 (6) ◽  
pp. 1869-1872 ◽  
Author(s):  
Maria Vittoria Spanedda ◽  
Béatrice Heurtault ◽  
Steffen Weidner ◽  
Corinne Baehr ◽  
Emmanuelle Boeglin ◽  
...  

2020 ◽  
Author(s):  
Yunkai Wang ◽  
Jie Wang ◽  
Lu Han ◽  
Yun Li Shen ◽  
Jie Yun You ◽  
...  

Abstract Background: Triggering receptor expressed on myeloid cells (TREM)-1is identified as a major upstream proatherogenic receptor. However, the cellular processes modulated by TREM-1 in the development of atherosclerosis and plaque destabilization has not been fully elucidated. In this study, we investigated the effects of TREM-1 on dendritic cell maturation and dendritic cell–mediated T-cell activation induced by oxidized low-density lipoprotein (ox-LDL) in atherogenesis. Methods: Human peripheral blood monocytes were differentiated to dendritic cells and stimulated by ox-LDL. Naive autologous T cells were co-cultured with pretreated dendritic cells.The expressionof TREM-1 and the production of inflammatory cytokines were assessed by real-time PCR, western blot and ELISA.The expression of immune factors was determined with FACS to evaluate dendritic cell maturation and T-cell activation. Results: Stimulation with ox-LDL promoted dendritic cell maturation, TREM-1 expression and T-cell activation, and exposure of T cells to ox-LDL-treated dendritic cells induced production of interferon-γ and IL-17. Blocking TREM-1 suppressed dendritic cell maturation with low expression of CD1a, CD40, CD86 and HLA-DR, decreased production of TNF-α, IL-1β, IL-6 and MCP-1, and increased secretion of TGF-β and IL-10. In addition, stimulation of ox-LDL induced miR-155, miR-27, Let-7c and miR-185 expression, whereas inhibition of TREM-1 repressed miRNA-155. Silencing TREM-1 or miRNA-155 increased SOCS1 expression induced by ox-LDL. T cells derived from carotid atherosclerotic plaques or healthy individuals showed similar result patterns. Conclusion: These data suggest that TREM-1 modulates maturation of dendritic cells and activation of plaque T cells induced by ox-LDL, a pivotal player in atherogenesis.


2019 ◽  
Vol 15 (8) ◽  
pp. e1007970 ◽  
Author(s):  
Kai Qin ◽  
Sushma Boppana ◽  
Victor Y. Du ◽  
Jonathan M. Carlson ◽  
Ling Yue ◽  
...  

2016 ◽  
Vol 100 (5) ◽  
pp. 855-864 ◽  
Author(s):  
D. M. Elizondo ◽  
T. E. Andargie ◽  
K. M. Marshall ◽  
A. M. Zariwala ◽  
M. W. Lipscomb

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