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

. 2021 Jul 19;9:697632. doi: 10.3389/fped.2021.697632

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

Copyright © 2021 Chang, Yang, Lin and Yang.

This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

PMC Copyright notice

Perspective of immunotherapies for KD refractory to conventional treatment. (1) Targeting the cytokine storm: Anti-TNF-α and anti-IL-1 have been used to rescue IVIG resistance. In addition, other Th17 and Th1 cytokines are also candidates for therapeutic targets. (2) Addressing the Th17/Treg imbalance can be achieved by augmentation of Th2 or Treg polarization, including the enhancement of FoxP3 expression. (3) Blockade or immunoregulation by allotypic and idiotypic IgG provides immunoregulation of KD. (4) Enhancement of immunoinhibitory receptors transduces the immunoreceptor tyrosine-based inhibitory motif (ITIM) to inhibit cytokine production. (5) Targeting the signal transduction of mitogen-activated protein kinases (MAPK) including p38 phosphorylation to suppress cytokine (TNF-α, IL-6, IL-1, etc.) production. (6) Screening genetic variants related to KD with IVIG resistance protects KD patients from coronary complications. (7) Epigenetic regulation of Treg immune responses reverses the Th17/Treg imbalance in KD with IVIG resistance. (8) Anti-hemophagocytosis can be achieved by targeting IFN-γ and TNF-α as well as the inhibition of their downstream effector STAT-1 (signal transducer and activator of transcription 1) or nitric oxide (NO) synthase activation (→ indicates activation; ⊥ indicates inhibitory regulation; - - -> indicates epigenetic regulation).