scholarly journals Found in translation: the human equivalent of mouse CD8+ dendritic cells

2010 ◽  
Vol 207 (6) ◽  
pp. 1131-1134 ◽  
Author(s):  
Jose A. Villadangos ◽  
Ken Shortman
Keyword(s):  
Dendritic Cells ◽  
Dendritic Cell ◽  
Cross Presentation ◽  
Cell Network

The murine dendritic cell network comprises multiple subsets with distinct functions, but few of their human counterparts have been described. New data now reveals the likely human equivalent of the mouse DC subset specialized in cross-presentation.

scholarly journals PYR-41 and Thalidomide Impair Dendritic Cell Cross-Presentation by Inhibiting Myddosome Formation and Attenuating the Endosomal Recruitments of p97 and Sec61 via NF-κB Inactivation

2018 ◽  
Vol 2018 ◽  
pp. 1-14 ◽  
Author(s):  
Xiang You ◽  
Dan Dan Xu ◽  
Di Zhang ◽  
Jie Chen ◽  
Feng Guang Gao
Keyword(s):  
T Cells ◽  
Dendritic Cells ◽  
Dendritic Cell ◽  
Side Effects ◽  
Protective Immunity ◽  
Therapeutic Effects ◽  
Cross Presentation ◽  
Associated Diseases

PYR-41 and thalidomide have therapeutic effects on inflammation-associated diseases with side effects such as tumorigenesis. Cross-presentation allows dendritic cells (DC) to present endogenous antigen and induce protective immunity against microbe infection and tumors. But, up to now, the effects of PYR-41 and thalidomide on cross-presentation are still uncertain. In this study, we investigated the effect and mechanism of PYR-41 and thalidomide on DC cross-presentation by observing Myddosome formation, endosomal recruitment of p97 and Sec61, NF-κB activation, and cross-priming ability. We demonstrated that the inhibition of endosomal recruitment of p97 and Sec61, together with attenuated NF-κB activation and Myddosome formation, contributes to PYR-41- and thalidomide-impaired cross-presentation and thereby reverses cross-activation of T cells. These observations suggest that NF-κB signaling and p97 and Sec61 molecules are candidates for dealing with the side effects of PYR-41 and thalidomide.

scholarly journals Modular expression analysis reveals functional conservation between human Langerhans cells and mouse cross-priming dendritic cells

2015 ◽  
Vol 212 (5) ◽  
pp. 743-757 ◽  
Author(s):  
Maxim N. Artyomov ◽  
Adiel Munk ◽  
Laurent Gorvel ◽  
Daniel Korenfeld ◽  
Marina Cella ◽  
...  
Keyword(s):  
Dendritic Cells ◽  
Dendritic Cell ◽  
Therapeutic Target ◽  
Langerhans Cells ◽  
Antigen Processing ◽  
Genome Project ◽  
Cross Presentation ◽  
Functional Conservation ◽  
Transcriptional Signature

Characterization of functionally distinct dendritic cell (DC) subsets in mice has fueled interest in whether analogous counterparts exist in humans. Transcriptional modules of coordinately expressed genes were used for defining shared functions between the species. Comparing modules derived from four human skin DC subsets and modules derived from the Immunological Genome Project database for all mouse DC subsets revealed that human Langerhans cells (LCs) and the mouse XCR1+CD8α+CD103+ DCs shared the class I–mediated antigen processing and cross-presentation transcriptional modules that were not seen in mouse LCs. Furthermore, human LCs were enriched in a transcriptional signature specific to the blood cross-presenting CD141/BDCA-3+ DCs, the proposed equivalent to mouse CD8α+ DCs. Consistent with our analysis, LCs were highly adept at inducing primary CTL responses. Thus, our study suggests that the function of LCs may not be conserved between mouse and human and supports human LCs as an especially relevant therapeutic target.

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