scholarly journals A polysaccharide derived from Lentinus edodes impairs the immunosuppressive function of myeloid-derived suppressor cells via the p38 pathways

RSC Advances ◽  
2017 ◽  
Vol 7 (58) ◽  
pp. 36533-36540 ◽  
Author(s):  
Jun Du ◽  
Ruijie Wang ◽  
Wensheng Zhang ◽  
Chao Zhang ◽  
Xiao Li ◽  
...  

MPSSS may reverse the function of the MSC2 cells through p38 activation and ERK suppression and provide a novel anti-cancer strategy by targeting myeloid immune suppressor cells.

Open Biology ◽  
2021 ◽  
Vol 11 (11) ◽  
Author(s):  
Mahmoud Mohammad Yaseen ◽  
Nizar Mohammad Abuharfeil ◽  
Homa Darmani

There are several mechanisms by which human immunodeficiency virus (HIV) can mediate immune dysfunction and exhaustion during the course of infection. Chronic immune activation, after HIV infection, seems to be a key driving force of such unwanted consequences, which in turn worsens the pathological status. In such cases, the immune system is programmed to initiate responses that counteract unwanted immune activation, for example through the expansion of myeloid-derived suppressor cells (MDSCs). Although the expansion of immune suppressor cells in the setting of systemic chronic immune activation, in theory, is expected to contain immune activation, HIV infection is still associated with a remarkably high level of biomarkers of immune activation. Paradoxically, the expansion of immune suppressor cells during HIV infection can suppress potent anti-viral immune responses, which in turn contribute to viral persistence and disease progression. This indicates that HIV hijacks not only immune activation but also the immune regulatory responses to its advantage. In this work, we aim to pave the way to comprehend how such unwanted expansion of MDSCs could participate in the pathology of acute/primary and chronic HIV infection in humans, as well as simian immunodeficiency virus infection in rhesus macaques, according to the available literature.


2011 ◽  
Vol 19 (1) ◽  
pp. 140-149 ◽  
Author(s):  
Candice Willmon ◽  
Rosa M Diaz ◽  
Phonphimon Wongthida ◽  
Feorillo Galivo ◽  
Timothy Kottke ◽  
...  

2020 ◽  
Vol 21 (21) ◽  
pp. 8412
Author(s):  
Jan Korbecki ◽  
Klaudyna Kojder ◽  
Donata Simińska ◽  
Romuald Bohatyrewicz ◽  
Izabela Gutowska ◽  
...  

CC chemokines, a subfamily of 27 chemotactic cytokines, are a component of intercellular communication, which is crucial for the functioning of the tumor microenvironment. Although many individual chemokines have been well researched, there has been no comprehensive review presenting the role of all known human CC chemokines in the hallmarks of cancer, and this paper aims at filling this gap. The first part of this review discusses the importance of CCL1, CCL3, CCL4, CCL5, CCL18, CCL19, CCL20, CCL21, CCL25, CCL27, and CCL28 in cancer. Here, we discuss the significance of CCL2 (MCP-1), CCL7, CCL8, CCL11, CCL13, CCL14, CCL15, CCL16, CCL17, CCL22, CCL23, CCL24, and CCL26. The presentation of each chemokine includes its physiological function and then the role in tumor, including proliferation, drug resistance, migration, invasion, and organ-specific metastasis of tumor cells, as well as the effects on angiogenesis and lymphangiogenesis. We also discuss the effects of each CC chemokine on the recruitment of cancer-associated cells to the tumor niche (eosinophils, myeloid-derived suppressor cells (MDSC), tumor-associated macrophages (TAM), tumor-associated neutrophils (TAN), regulatory T cells (Treg)). On the other hand, we also present the anti-cancer properties of CC chemokines, consisting in the recruitment of tumor-infiltrating lymphocytes (TIL).


PLoS ONE ◽  
2012 ◽  
Vol 7 (12) ◽  
pp. e51751 ◽  
Author(s):  
Hao Wu ◽  
Ning Tao ◽  
Xiaoman Liu ◽  
Xiao Li ◽  
Jian Tang ◽  
...  

Sign in / Sign up

Export Citation Format

Share Document