Cellular networks controlling Th2 polarization in allergy and immunity
In contrast to the development of Th1 (type 1 T helper cells), Th17 and Treg (regulatory T cells), little is known of the mechanisms governing Th2 development, which is important for immunity to helminths and for us to understand the pathogenesis of allergy. A picture is emerging in which mucosal ep...
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pubmed-32922862012-03-08 Cellular networks controlling Th2 polarization in allergy and immunity Kool, Mirjam Hammad, Hamida Lambrecht, Bart N. Review Article In contrast to the development of Th1 (type 1 T helper cells), Th17 and Treg (regulatory T cells), little is known of the mechanisms governing Th2 development, which is important for immunity to helminths and for us to understand the pathogenesis of allergy. A picture is emerging in which mucosal epithelial cells instruct dendritic cells to promote Th2 responses in the absence of IL-12 (interleukin 12) production and provide instruction through thymic stromal lymphopoieitin (TSLP) or granulocyte-macrophage colony stimulating factor (GM-CSF). At the same time, allergens, helminths and chemical adjuvants elicit the response of innate immune cells like basophils, which provide more polarizing cytokines and IL-4 and reinforce Th2 immunity. This unique communication between cells will only be fully appreciated if we study Th2 immunity in vivo and in a tissue-specific context, and can only be fully understood if we compare several models of Th2 immune response induction. Faculty of 1000 Ltd 2012-03-01 /pmc/articles/PMC3292286/ /pubmed/22403589 http://dx.doi.org/10.3410/B4-6 Text en © 2012 Faculty of 1000 Ltd http://creativecommons.org/licenses/by-nc/3.0/legalcode This is an open-access article distributed under the terms of the Creative Commons Attribution-Non Commercial License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. You may not use this work for commercial purposes |
repository_type |
Open Access Journal |
institution_category |
Foreign Institution |
institution |
US National Center for Biotechnology Information |
building |
NCBI PubMed |
collection |
Online Access |
language |
English |
format |
Online |
author |
Kool, Mirjam Hammad, Hamida Lambrecht, Bart N. |
spellingShingle |
Kool, Mirjam Hammad, Hamida Lambrecht, Bart N. Cellular networks controlling Th2 polarization in allergy and immunity |
author_facet |
Kool, Mirjam Hammad, Hamida Lambrecht, Bart N. |
author_sort |
Kool, Mirjam |
title |
Cellular networks controlling Th2 polarization in allergy and immunity |
title_short |
Cellular networks controlling Th2 polarization in allergy and immunity |
title_full |
Cellular networks controlling Th2 polarization in allergy and immunity |
title_fullStr |
Cellular networks controlling Th2 polarization in allergy and immunity |
title_full_unstemmed |
Cellular networks controlling Th2 polarization in allergy and immunity |
title_sort |
cellular networks controlling th2 polarization in allergy and immunity |
description |
In contrast to the development of Th1 (type 1 T helper cells), Th17 and Treg (regulatory T cells), little is known of the mechanisms governing Th2 development, which is important for immunity to helminths and for us to understand the pathogenesis of allergy. A picture is emerging in which mucosal epithelial cells instruct dendritic cells to promote Th2 responses in the absence of IL-12 (interleukin 12) production and provide instruction through thymic stromal lymphopoieitin (TSLP) or granulocyte-macrophage colony stimulating factor (GM-CSF). At the same time, allergens, helminths and chemical adjuvants elicit the response of innate immune cells like basophils, which provide more polarizing cytokines and IL-4 and reinforce Th2 immunity. This unique communication between cells will only be fully appreciated if we study Th2 immunity in vivo and in a tissue-specific context, and can only be fully understood if we compare several models of Th2 immune response induction. |
publisher |
Faculty of 1000 Ltd |
publishDate |
2012 |
url |
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3292286/ |
_version_ |
1611510046422728704 |