scholarly journals Regulation of Adaptive Immunity by the Innate Immune System

Science ◽  
2010 ◽  
Vol 327 (5963) ◽  
pp. 291-295 ◽  
Author(s):  
A. Iwasaki ◽  
R. Medzhitov
Keyword(s):  
Immune System ◽  
Adaptive Immunity ◽  
Innate Immune System ◽  
Innate Immune

scholarly journals Insights into Sensing of Murine Retroviruses

Viruses ◽  
2020 ◽  
Vol 12 (8) ◽  
pp. 836
Author(s):  
Eileen A. Moran ◽  
Susan R. Ross
Keyword(s):  
Immune Response ◽  
Immune System ◽  
Nucleic Acid ◽  
Adaptive Immunity ◽  
Innate Immune System ◽  
Innate Immune ◽  
Genetic Tool ◽  
Causes Of Disease ◽  
Retrovirus Infection ◽  
Insight Into

Retroviruses are major causes of disease in animals and human. Better understanding of the initial host immune response to these viruses could provide insight into how to limit infection. Mouse retroviruses that are endemic in their hosts provide an important genetic tool to dissect the different arms of the innate immune system that recognize retroviruses as foreign. Here, we review what is known about the major branches of the innate immune system that respond to mouse retrovirus infection, Toll-like receptors and nucleic acid sensors, and discuss the importance of these responses in activating adaptive immunity and controlling infection.

Abstract 526: Cancer immunoediting by the innate immune system in the absence of adaptive immunity

2012 ◽  
Author(s):  
Jack Bui ◽  
Timothy O'Sullivan ◽  
Robert Saddawi-Konefka ◽  
William Vermi ◽  
Mark Smyth ◽  
...  
Keyword(s):  
Immune System ◽  
Adaptive Immunity ◽  
Innate Immune System ◽  
Innate Immune ◽  
Cancer Immunoediting

scholarly journals Control of adaptive immunity by the innate immune system

2015 ◽  
Vol 16 (4) ◽  
pp. 343-353 ◽  
Author(s):  
Akiko Iwasaki ◽  
Ruslan Medzhitov
Keyword(s):  
Immune System ◽  
Adaptive Immunity ◽  
Innate Immune System ◽  
Innate Immune

scholarly journals NOD1 and NOD2 receptors: integral members of the innate and adaptive immunity system.

2013 ◽  
Vol 60 (3) ◽  
Author(s):  
Halina Antosz ◽  
Magdalena Osiak
Keyword(s):  
Immune System ◽  
Signaling Pathways ◽  
Adaptive Immunity ◽  
Innate Immune System ◽  
Inflammatory Diseases ◽  
Innate Immune ◽  
Inflammatory Signaling ◽  
Innate And Adaptive Immunity ◽  
Essential Component

NOD-like proteins (NLR) are a specialized group of intracellular receptors, which constitute an essential component of the host innate immune system. They were discovered more than a decade ago, but research on this particular class of microbial detectors is still ongoing to allow for a better understanding of the mechanisms, recognition of microorganisms, transmission of signals, and carrying out the activation of inflammatory signaling pathways. In this review, we discuss the construction of NOD1 and NOD2 receptors, their functions, and significance in the pathogenesis of inflammatory diseases in humans.

scholarly journals Cancer immunoediting by the innate immune system in the absence of adaptive immunity

2012 ◽  
Vol 209 (10) ◽  
pp. 1869-1882 ◽  
Author(s):  
Timothy O’Sullivan ◽  
Robert Saddawi-Konefka ◽  
William Vermi ◽  
Catherine M. Koebel ◽  
Cora Arthur ◽  
...  
Keyword(s):  
Immune System ◽  
Adaptive Immunity ◽  
Immune Cells ◽  
Innate Immune System ◽  
Nk Cell ◽  
Interferon Γ ◽  
Innate Immune ◽  
M1 Macrophages ◽  
Cancer Immunoediting ◽  
Ifn Γ

Cancer immunoediting is the process whereby immune cells protect against cancer formation by sculpting the immunogenicity of developing tumors. Although the full process depends on innate and adaptive immunity, it remains unclear whether innate immunity alone is capable of immunoediting. To determine whether the innate immune system can edit tumor cells in the absence of adaptive immunity, we compared the incidence and immunogenicity of 3′methylcholanthrene-induced sarcomas in syngeneic wild-type, RAG2−/−, and RAG2−/−x γc−/− mice. We found that innate immune cells could manifest cancer immunoediting activity in the absence of adaptive immunity. This activity required natural killer (NK) cells and interferon γ (IFN-γ), which mediated the induction of M1 macrophages. M1 macrophages could be elicited by administration of CD40 agonists, thereby restoring editing activity in RAG2−/−x γc−/− mice. Our results suggest that in the absence of adaptive immunity, NK cell production of IFN-γ induces M1 macrophages, which act as important effectors during cancer immunoediting.

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