An allergenic plant calmodulin from Artemisia pollen primes human DCs leads to Th2 polarization

Artemisia pollen is the major cause of seasonal allergic respiratory diseases in the northern hemisphere. About 28.57% of Artemisia allergic patients’ IgE can recognize ArtCaM, a novel allergenic calmodulin from Artemisia identified in this study. These patients exhibited stronger allergic reactions...

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Published in:Frontiers in immunology Vol. 13; p. 996427
Main Authors: Zhang, Yue, Hu, Wenzhi, Chen, Dongbo, Ding, Ming, Wang, Tao, Wang, Yaojun, Chi, Jiaoni, Li, Zhimin, Li, Qiang, Li, Chengxin
Format: Journal Article
Language:English
Published: Frontiers Media S.A 29-09-2022
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Summary:Artemisia pollen is the major cause of seasonal allergic respiratory diseases in the northern hemisphere. About 28.57% of Artemisia allergic patients’ IgE can recognize ArtCaM, a novel allergenic calmodulin from Artemisia identified in this study. These patients exhibited stronger allergic reactions and a longer duration of allergic symptoms. However, the signaling mechanism that triggers these allergic reactions is not fully understood. In this study, we found that extracellular ArtCaM directly induces the maturation of human dendritic cells (DCs), which is attributed to a series of Ca 2+ relevant cascades, including Ca 2+ /NFAT/CaMKs. ArtCaM alone induces inflammatory response toward Th1, Th17, and Treg. Interestingly, a combination of ArtCaM and anti-ArtCaM IgE led to Th2 polarization. The putative mechanism is that anti-ArtCaM IgE partially blocks the ArtCaM-induced ERK signal, but does not affect Ca 2+ -dependent cascades. The crosstalk between ERK and Ca 2+ signal primes DCs maturation and Th2 polarization. In summary, ArtCaM related to clinical symptoms when combined with anti-ArtCaM IgE, could be a novel allergen to activate DCs and promote Th2 polarization. Such findings provide mechanistic insights into Th2 polarization in allergic sensitization and pave the way for novel preventive and therapeutic strategies for efficient management of such pollen allergic disease.
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This article was submitted to Antigen Presenting Cell Biology, a section of the journal Frontiers in Immunology
These authors have contributed equally to this work and share first authorship
Edited by: Efstratios Stratikos, National and Kapodistrian University of Athens, Greece
Reviewed by: Seung-Hyo Lee, Korea Advanced Institute of Science and Technology, South Korea; George Bertsias, University of Crete, Greece
ISSN:1664-3224
1664-3224
DOI:10.3389/fimmu.2022.996427