Open AccessInterleukin-22 (IL-22) Binding Protein Constrains IL-22 Activity, Host Defense, and Oxidative Phosphorylation Genes during Pneumococcal Pneumonia
Author(s) -
Giraldina Trevejo-Nuñez,
Waleed Elsegeiny,
Felix E.Y. Aggor,
Jamie L. Tweedle,
Zoe Kaplan,
Pranali Gandhi,
Patricia Castillo,
Annabel A. Ferguson,
John F. Alcorn,
Kong Chen,
Jay K. Kolls,
Sarah L. Gaffen
Publication year - 2019
Publication title -
infection and immunity
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.508
H-Index - 220
eISSN - 1070-6313
pISSN - 0019-9567
DOI - 10.1128/iai.00550-19
Subject(s) - biology , downregulation and upregulation , streptococcus pneumoniae , immunology , interleukin 10 , microbiology and biotechnology , pneumococcal infections , proinflammatory cytokine , pneumococcal pneumonia , phagocytosis , complement system , interleukin 22 , oxidative phosphorylation , interleukin , inflammation , gene , immune system , cytokine , biochemistry , antibiotics
Streptococcus pneumoniae is the most common cause of community-acquired pneumonia worldwide, and interleukin-22 (IL-22) helps contain pneumococcal burden in lungs and extrapulmonary tissues. Administration of IL-22 increases hepatic complement 3 and complement deposition on bacteria and improves phagocytosis by neutrophils. The effects of IL-22 can be tempered by a secreted natural antagonist, known as IL-22 binding protein (IL-22BP), encoded byIl22ra2 .
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