On the origins of adaptive immunity: innate immune receptors join the tale

2004 ◽  
Vol 25 (1) ◽  
pp. 11-16 ◽  
Author(s):  
T VANDENBERG ◽  
J YODER ◽  
G LITMAN
Keyword(s):  
Adaptive Immunity ◽  
Innate Immune ◽  
Immune Receptors

scholarly journals Coordinated Neutralization and Immune Activation by the Cytosolic Antibody Receptor TRIM21

2016 ◽  
Vol 90 (10) ◽  
pp. 4856-4859 ◽  
Author(s):  
Adam J. Fletcher ◽  
Leo C. James
Keyword(s):  
Recent Work ◽  
Adaptive Immunity ◽  
Immune Activation ◽  
Mammalian Cells ◽  
Antiviral Response ◽  
Innate Immune ◽  
High Affinity ◽  
Immune Receptors ◽  
Intracellular Environment ◽  
Shed Light

TRIM21 is a high-affinity antibody receptor uniquely expressed in the cytosol of mammalian cells. Here we summarize its role in extending antibody protection into the intracellular environment and allowing nonprofessional cells to benefit from adaptive immunity. We highlight recent work that has shed light on how TRIM21 acts as both an immune sensor and effector. We also review how TRIM21 synergizes with other innate immune receptors to promote an integrated antiviral response.

scholarly journals Effects of innate immune receptor stimulation on extracellular α-synuclein uptake and degradation by brain resident cells

2021 ◽  
Author(s):  
Changyoun Kim ◽  
Somin Kwon ◽  
Michiyo Iba ◽  
Brian Spencer ◽  
Edward Rockenstein ◽  
...  
Keyword(s):  
Degradation Kinetics ◽  
Morphological Changes ◽  
Direct Interaction ◽  
Innate Immune ◽  
Pathological Feature ◽  
Tlr2 Expression ◽  
Immune Receptors ◽  
Age Related ◽  
Stimulation Of

AbstractSynucleinopathies are age-related neurological disorders characterized by the progressive deposition of α-synuclein (α-syn) aggregates and include Parkinson’s disease (PD) and dementia with Lewy bodies (DLB). Although cell-to-cell α-syn transmission is thought to play a key role in the spread of α-syn pathology, the detailed mechanism is still unknown. Neuroinflammation is another key pathological feature of synucleinopathies. Previous studies have identified several immune receptors that mediate neuroinflammation in synucleinopathies, such as Toll-like receptor 2 (TLR2). However, the species of α-syn aggregates varies from study to study, and how different α-syn aggregate species interact with innate immune receptors has yet to be addressed. Therefore, we investigated whether innate immune receptors can facilitate the uptake of different species of α-syn aggregates. Here, we examined whether stimulation of TLRs could modulate the cellular uptake and degradation of α-syn fibrils despite a lack of direct interaction. We observed that stimulation of TLR2 in vitro accelerated α-syn fibril uptake in neurons and glia while delaying the degradation of α-syn in neurons and astrocytes. Internalized α-syn was rapidly degraded in microglia regardless of whether TLR2 was stimulated. However, cellular α-syn uptake and degradation kinetics were not altered by TLR4 stimulation. In addition, upregulation of TLR2 expression in a synucleinopathy mouse model increased the density of Lewy-body-like inclusions and induced morphological changes in microglia. Together, these results suggest that cell type-specific modulation of TLR2 may be a multifaceted and promising therapeutic strategy for synucleinopathies; inhibition of neuronal and astroglial TLR2 decreases pathogenic α-syn transmission, but activation of microglial TLR2 enhances microglial extracellular α-syn clearance.

Dysregulation of innate immune receptors on neutrophils in chronic granulomatous disease

2008 ◽  
Vol 121 (2) ◽  
pp. 375-382.e9 ◽  
Author(s):  
Dominik Hartl ◽  
Natalie Lehmann ◽  
Florian Hoffmann ◽  
Annette Jansson ◽  
Andreas Hector ◽  
...  
Keyword(s):  
Chronic Granulomatous Disease ◽  
Innate Immune ◽  
Granulomatous Disease ◽  
Immune Receptors

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
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