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

. 2019 Nov 14;217(1):e20191397. doi: 10.1084/jem.20191397

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

© 2019 Prinz et al.

This article is distributed under the terms of an Attribution–Noncommercial–Share Alike–No Mirror Sites license for the first six months after the publication date (see http://www.rupress.org/terms/). After six months it is available under a Creative Commons License (Attribution–Noncommercial–Share Alike 4.0 International license, as described at https://creativecommons.org/licenses/by-nc-sa/4.0/).

PMC Copyright notice

Figure 2. — IL-17 immunity in human psoriasis. (A) Psoriasis pathogenesis is induced by increased levels of IL-17 that stimulate keratinocyte proliferation resulting in acanthosis, para- and hyperkeratosis, and release of AMP and chemokines that recruit neutrophils from the circulation, leading to formation of Munro’s microabscesses within the stratum corneum. Increased IL-23/IL-17 levels can be caused by presentation of autoantigens by melanocytes to autoreactive epidermal CD8⁺ T cells resulting in IL-17 secretion and by plasmacytoid DCs (pDCs) activated by antimicrobial peptide (AMP)–nucleic acid complexes to secrete type I interferons that in turn induce secretion of IL-23 by dermal DCs subsequently stimulating and recruiting IL-17 producing lymphoid cells. (B) Targeting IL-23, IL-17, and/or IL-17R by specific mAb leads to less stimulation of keratinocytes and IL-17–secreting cells. This results in reduced acanthosis, inhibits infiltration of neutrophils, and thus ameliorates psoriasis pathology.