Bibliographic Details
| Title: |
Human monocyte-derived type 1 and 2 macrophages recognize Ara h 1, a major peanut allergen, by different mechanisms |
| Authors: |
Maren Krause, Peter Crauwels, Frank Blanco-Pérez, Martin Globisch, Andrea Wangorsch, Thomas Henle, Jonas Lidholm, Ger van Zandbergen, Stefan Vieths, Stephan Scheurer, Masako Toda |
| Source: |
Scientific Reports, Vol 11, Iss 1, Pp 1-13 (2021) |
| Publisher Information: |
Nature Portfolio, 2021. |
| Publication Year: |
2021 |
| Collection: |
LCC:Medicine
LCC:Science |
| Subject Terms: |
Medicine, Science |
| More Details: |
Abstract Evidence has suggested that major peanut allergen Ara h 1 activates dendritic cells (DCs) via interaction with DC-SIGN (dendritic cell-specific intercellular adhesion molecule-3-grabbing non-integrin), a C-type lectin receptor, and contributes to development of peanut allergy. Since macrophages, as well as DCs, play a crucial role in innate immunity, we investigated whether natural Ara h 1 (nAra h 1) activates two different subsets of macrophages, human monocyte derived macrophage type 1 (hMDM1: pro-inflammatory model) and type 2 (hMDM2: anti-inflammatory model). hMDM1 and hMDM2 predominantly produced pro-inflammatory cytokines (IL-6 and TNF-α) and an anti-inflammatory cytokine (IL-10) in response to nAra h 1, respectively. hMDM2 took up nAra h 1 and expressed DC-SIGN at higher levels than hMDM1. However, small interfering RNA knockdown of DC-SIGN did not suppress nAra h 1 uptake and nAra h 1-mediated cytokine production in hMDM2. Inhibitors of scavenger receptor class A type I (SR-AI) suppressed the response of hMDM2, but not of hMDM1, suggesting that SR-AI is a major receptor in hMDM2 for nAra h 1 recognition and internalization. nAra h 1 appears to exert stimulatory capacity on DC and macrophages via different receptors. This study advances our understanding how a major peanut allergen interacts with innate immunity. |
| Document Type: |
article |
| File Description: |
electronic resource |
| Language: |
English |
| ISSN: |
2045-2322 |
| Relation: |
https://doaj.org/toc/2045-2322 |
| DOI: |
10.1038/s41598-021-89402-1 |
| Access URL: |
https://doaj.org/article/20c6e2aeda004d45aa57242365d95d6c |
| Accession Number: |
edsdoj.20c6e2aeda004d45aa57242365d95d6c |
| Database: |
Directory of Open Access Journals |
