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Title: The amphibian complement system and chytridiomycosis
Abstract

Understanding host immune function and ecoimmunology is increasingly important at a time when emerging infectious diseases (EIDs) threaten wildlife. One EID that has emerged and spread widely in recent years is chytridiomycosis, caused by the fungal pathogenBatrachochytrium dendrobatidis(Bd), which is implicated unprecedented amphibian declines around the world. The impacts ofBdhave been severe for many amphibian species, but some populations have exhibited signs of persistence, and even recovery, in some regions. Many mechanisms may underpin this pattern and amphibian immune responses are likely one key component. Although we have made great strides in understanding amphibian immunity, the complement system remains poorly understood. The complement system is a nonspecific, innate immune defense that is known to enhance other immune responses. Complement activation can occur by three different biochemical pathways and result in protective mechanisms, such as inflammation, opsonization, and pathogen lysis, thereby providing protection to the host. We currently lack an understanding of complement pathway activation for chytridiomycosis, but several studies have suggested that it may be a key part of an early and robust immune response that confers host resistance. Here, we review the available research on the complement system in general as well as amphibian complement responses toBdinfection. Additionally, we propose future research directions that will increase our understanding of the amphibian complement system and other immune responses toBd. Finally, we suggest how a deeper understanding of amphibian immunity could enhance the conservation and management of amphibian species that are threatened by chytridiomycosis.

 
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Award ID(s):
1846403
NSF-PAR ID:
10207265
Author(s) / Creator(s):
 ;  
Publisher / Repository:
Wiley Blackwell (John Wiley & Sons)
Date Published:
Journal Name:
Journal of Experimental Zoology Part A: Ecological and Integrative Physiology
Volume:
333
Issue:
10
ISSN:
2471-5638
Page Range / eLocation ID:
p. 706-719
Format(s):
Medium: X
Sponsoring Org:
National Science Foundation
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