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

Autor:	Zhang Y; Chinese PLA Medical School, Chinese PLA General Hospital, Beijing, China.; Department of Dermatology, Air Force Medical Center, PLA, Beijing, China.; Department of Dermatology, The First Medical Center of Chinese PLA General Hospital, Beijing, China., Hu W; Department of Dermatology, Air Force Medical Center, PLA, Beijing, China., Chen D; Peking University People's Hospital, Peking University Hepatology Institute, Beijing Key Laboratory of Hepatitis C and Immunotherapy for Liver Disease, Beijing, China., Ding M; Department of Dermatology, Air Force Medical Center, PLA, Beijing, China., Wang T; Department of Dermatology, Air Force Medical Center, PLA, Beijing, China., Wang Y; Department of Dermatology, Air Force Medical Center, PLA, Beijing, China., Chi J; Department of Dermatology, Air Force Medical Center, PLA, Beijing, China., Li Z; Department of Dermatology, Air Force Medical Center, PLA, Beijing, China., Li Q; Department of Dermatology, Air Force Medical Center, PLA, Beijing, China., Li C; Chinese PLA Medical School, Chinese PLA General Hospital, Beijing, China.; Department of Dermatology, The First Medical Center of Chinese PLA General Hospital, Beijing, China.
Jazyk:	angličtina
Zdroj:	Frontiers in immunology [Front Immunol] 2022 Sep 29; Vol. 13, pp. 996427. Date of Electronic Publication: 2022 Sep 29 (Print Publication: 2022).
DOI:	10.3389/fimmu.2022.996427
Abstrakt:	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. Competing Interests: The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest. (Copyright © 2022 Zhang, Hu, Chen, Ding, Wang, Wang, Chi, Li, Li and Li.)
Databáze:	MEDLINE
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