Figure - PMC

Skip to main content

An official website of the United States government

Here's how you know

Here's how you know

Official websites use .gov
A .gov website belongs to an official government organization in the United States.

Secure .gov websites use HTTPS
A lock ( ) or https:// means you've safely connected to the .gov website. Share sensitive information only on official, secure websites.

View full-text article in PMC

. 2020 Aug 31;10:36. doi: 10.1186/s13601-020-00341-y

Search in PMC
Search in PubMed
View in NLM Catalog
Add to search

© The Author(s) 2020

Open AccessThis article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit http://creativecommons.org/licenses/by/4.0/. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated in a credit line to the data.

PMC Copyright notice

Fig. 1 — Pollen-induced activation of the innate immune system and Th2 polarization. The initiation of allergic sensitization is a complex network of diverse immune cells, such as DCs, ILC2s and neutrophils. Upon encounter with the epithelium the pollen hydrates and releases its content including allergens and various other bioactive molecules (1). At the epithelium (2), this immunogenic cocktail causes the disruption of the epithelial membrane, activates PRRs such as TLR4 and PAR2, triggers the release of alarmins (TSLP, IL-25 and IL-33), and induces oxidative stress and secretion of IL-8 and other pro-inflammatory cytokines (IL-1, IL-6 and TNFα). In turn, DCs are activated (upregulation of surface markers including OX40L and notch ligands), migrate to the lymph nodes (expression of CXCR5), where they present processed antigens via MHC-II to naïve T cells (3). Th2 polarization occurs either STAT6/GATA-3/IL-4-dependent (4A) or -independent via the NF-κB/STAT5 pathway and the contribution of ILC2s (4B). The origin of initial IL-4 for Th2 polarization is still a matter of discussion; proposed candidate are basophils and NKT cells. Once a Th2 immune response has been initiated, a class-switch of B cells to antigen-specific IgE-producing plasma cells occurs resulting in the sensitization of susceptible individuals to pollen allergens (5). CCL17, CCL22 chemokine (C–C motif) ligand 17 and 22, CCR7 C–C chemokine receptor type 7, CD80, CD86 and CD40 cluster of differentiation 80, 86 and 40, CXCL-13 C-X-C motif chemokine 13, CXCR5 C-X-C chemokine receptor type 5, DCs dendritic cells, GATA-3 GATA binding protein 3, IL- Interleukin, ILC2 type 2 innate lymphoid cells, IRF4 interferon regulatory factor 4, NF-κB nuclear factor 'kappa-light-chain-enhancer' of activated B cells, NKT natural killer T, OX40L OX40 ligand, PARs protease activated receptors, PRRs pattern recognition receptors, ROS reactive oxygen species, ST2 IL-33 receptor, STAT5, STAT6 signal transducer and activator of transcription 5 and 6, Th T helper cells, TLR4 toll-like receptor 4, TNFα Tumor necrosis factor alpha, TSLP thymic stromal lymphopoietin