Asset Details
Do you wish to reserve the book?
Integrin CD11b activation drives anti-tumor innate immunity
Hey, we have placed the reservation for you!
By the way, why not check out events that you can attend while you pick your title.
Oops! Something went wrong.
Looks like we were not able to place the reservation. Kindly try again later.
Are you sure you want to remove the book from the shelf?
Integrin CD11b activation drives anti-tumor innate immunity
Do you wish to request the book?
Integrin CD11b activation drives anti-tumor innate immunity
Please be aware that the book you have requested cannot be checked out. If you would like to checkout this book, you can reserve another copy
We have requested the book for you!
Your request is successful and it will be processed during the Library working hours. Please check the status of your request in My Requests.
Oops! Something went wrong.
Looks like we were not able to place your request. Kindly try again later.
Journal Article
Integrin CD11b activation drives anti-tumor innate immunity
2018
Overview
Myeloid cells are recruited to damaged tissues where they can resolve infections and tumor growth or stimulate wound healing and tumor progression. Recruitment of these cells is regulated by integrins, a family of adhesion receptors that includes integrin CD11b. Here we report that, unexpectedly, integrin CD11b does not regulate myeloid cell recruitment to tumors but instead controls myeloid cell polarization and tumor growth. CD11b activation promotes pro-inflammatory macrophage polarization by stimulating expression of microRNA
Let7a
. In contrast, inhibition of CD11b prevents
Let7a
expression and induces cMyc expression, leading to immune suppressive macrophage polarization, vascular maturation, and accelerated tumor growth. Pharmacological activation of CD11b with a small molecule agonist, Leukadherin 1 (LA1), promotes pro-inflammatory macrophage polarization and suppresses tumor growth in animal models of murine and human cancer. These studies identify CD11b as negative regulator of immune suppression and a target for cancer immune therapy.
Recruitment of myeloid cells can be regulated by integrin CD11b. Here the authors show that in the tumor microenvironment, CD11b is not essential for recruitment of myeloid cells but rather induces macrophage anti-tumorigenic polarization via stimulating
let7a
and NFκB signaling and that pharmacological activation of CD11b enhances survival in mouse models of cancer.
Publisher
Nature Publishing Group UK,Nature Publishing Group,Nature Portfolio
Subject
/ 13/1
/ 13/106
/ 13/109
/ 13/21
/ 13/31
/ 13/51
/ 13/89
/ 13/95
/ 38
/ 38/77
/ 38/90
/ 59
/ 64
/ 64/60
/ Animals
/ Cancer
/ Humanities and Social Sciences
/ Immunity
/ Melanoma, Experimental - drug therapy
/ Melanoma, Experimental - immunology
/ miRNA
/ Neovascularization, Pathologic
/ Proto-Oncogene Proteins c-myc - metabolism
/ RNA
/ Roles
/ Science
/ Thiohydantoins - pharmacology
/ Thiohydantoins - therapeutic use
/ Tumors
