Saved in:
Bibliographic Details
Main Authors: Gao, Haiyou, Wei, Xiumei, Li, Kang, Cao, Yi, Rao, Wenzhuo, Zhang, Jiansong, Wang, Ding, Yang, Jialong
Format: Artículo científico
Language:en
Published: Proceedings of the National Academy of Sciences of the United States of America 2024
Subjects:
Online Access:https://pubmed.ncbi.nlm.nih.gov/39680767/
Tags: Add Tag
No Tags, Be the first to tag this record!
_version_ 1868266268220456960
author Gao, Haiyou
Wei, Xiumei
Li, Kang
Cao, Yi
Rao, Wenzhuo
Zhang, Jiansong
Wang, Ding
Yang, Jialong
author_facet Gao, Haiyou
Wei, Xiumei
Li, Kang
Cao, Yi
Rao, Wenzhuo
Zhang, Jiansong
Wang, Ding
Yang, Jialong
Gao, Haiyou
Wei, Xiumei
Li, Kang
Cao, Yi
Rao, Wenzhuo
Zhang, Jiansong
Wang, Ding
Yang, Jialong
collection PubMed - marine biology
contents Cold-blooded vertebrate utilizes behavioral fever to alleviate T cell apoptosis and optimize antimicrobial immunity. Gao, Haiyou Wei, Xiumei Li, Kang Cao, Yi Rao, Wenzhuo Zhang, Jiansong Wang, Ding Yang, Jialong Animals Apoptosis T-Lymphocytes Cichlids Enterobacteriaceae Infections Fish Diseases Immunity, Innate Adaptive Immunity HSP70 Heat-Shock Proteins Fever Fever confers significant survival benefits on endotherms by optimizing both innate and adaptive immunity. Ectotherms achieve thermoregulation using behavioral strategies, but existing evidence supports its enhancement effect on innate immunity only. Therefore, it remains unknown whether the coordination between fever and adaptive immunity was independently acquired by endotherms or instead represents a gradually evolved function common to vertebrates. In the present study, we reported that Nile tilapia developed behavioral fever to enhance the immune response against infection. Behavioral fever lasted five days, and the immune potential was optimized at 4 to 6 d post infection, indicating a potential correlation between fever events and T cell immunity. Further investigation suggested that fever did not affect T cell activation or proliferation but improved the ability of T cells to produce IFN-γ and Granzyme B and enhanced cytotoxicity, thereby eliminating the infection more effectively. Notably, we identified an advantage conferred by fever during infection: alleviation of T cell apoptosis to maintain a considerable T cell pool. Mechanistically, fever induced the expression of HSP70, which in turn entered the nucleus and bound to and promoted the phosphorylation of ERK1/2, thereby inhibiting the cleavage of caspase-8/caspase-3 and preventing T cell apoptosis. Our findings elucidate the detailed mechanism by which behavioral fever optimizes T cell immunity in a cold-blooded vertebrate and propose that integrating fever with adaptive immunity to gain survival advantages is an ancient strategy acquired before the emergence of tetrapod.
format Artículo científico
id pubmed_39680767
institution PubMed
language en
publishDate 2024
publisher Proceedings of the National Academy of Sciences of the United States of America
record_format pubmed
spellingShingle Cold-blooded vertebrate utilizes behavioral fever to alleviate T cell apoptosis and optimize antimicrobial immunity.
Gao, Haiyou
Wei, Xiumei
Li, Kang
Cao, Yi
Rao, Wenzhuo
Zhang, Jiansong
Wang, Ding
Yang, Jialong
Animals
Apoptosis
T-Lymphocytes
Cichlids
Enterobacteriaceae Infections
Fish Diseases
Immunity, Innate
Adaptive Immunity
HSP70 Heat-Shock Proteins
Fever
Cold-blooded vertebrate utilizes behavioral fever to alleviate T cell apoptosis and optimize antimicrobial immunity. Gao, Haiyou Wei, Xiumei Li, Kang Cao, Yi Rao, Wenzhuo Zhang, Jiansong Wang, Ding Yang, Jialong Animals Apoptosis T-Lymphocytes Cichlids Enterobacteriaceae Infections Fish Diseases Immunity, Innate Adaptive Immunity HSP70 Heat-Shock Proteins Fever Fever confers significant survival benefits on endotherms by optimizing both innate and adaptive immunity. Ectotherms achieve thermoregulation using behavioral strategies, but existing evidence supports its enhancement effect on innate immunity only. Therefore, it remains unknown whether the coordination between fever and adaptive immunity was independently acquired by endotherms or instead represents a gradually evolved function common to vertebrates. In the present study, we reported that Nile tilapia developed behavioral fever to enhance the immune response against infection. Behavioral fever lasted five days, and the immune potential was optimized at 4 to 6 d post infection, indicating a potential correlation between fever events and T cell immunity. Further investigation suggested that fever did not affect T cell activation or proliferation but improved the ability of T cells to produce IFN-γ and Granzyme B and enhanced cytotoxicity, thereby eliminating the infection more effectively. Notably, we identified an advantage conferred by fever during infection: alleviation of T cell apoptosis to maintain a considerable T cell pool. Mechanistically, fever induced the expression of HSP70, which in turn entered the nucleus and bound to and promoted the phosphorylation of ERK1/2, thereby inhibiting the cleavage of caspase-8/caspase-3 and preventing T cell apoptosis. Our findings elucidate the detailed mechanism by which behavioral fever optimizes T cell immunity in a cold-blooded vertebrate and propose that integrating fever with adaptive immunity to gain survival advantages is an ancient strategy acquired before the emergence of tetrapod.
title Cold-blooded vertebrate utilizes behavioral fever to alleviate T cell apoptosis and optimize antimicrobial immunity.
topic Animals
Apoptosis
T-Lymphocytes
Cichlids
Enterobacteriaceae Infections
Fish Diseases
Immunity, Innate
Adaptive Immunity
HSP70 Heat-Shock Proteins
Fever
url https://pubmed.ncbi.nlm.nih.gov/39680767/