| Literature DB >> 31475084 |
Fei Ye1,2, Qijian He1, Yan Wang1, Can Cui1, Fuling Yang1, Bin Luo1, Huadong Yin1, Xiaoling Zhao1, Diyan Li1, Hengyong Xu1, Hua Li1,2, Qing Zhu1.
Abstract
Immunosuppression caused by avian leukemia virus J subgroup (ALV-J) infection includes atrophy or regeneration disorders of the lymphoid organs, decreased immune response, and termination of B lymphocyte maturation process and inhibition of T-lymphocyte development. The regulatory mechanism of the related resistance genes and protein expression is not clear. While searching for a molecular marker for the immune response to ALV-J infection, we detected differentially expressed proteins (DEPs) of spleens from chicken infected by ALV-J at 15th day and 30th day by the data-independent acquisition technique. Approximately 220 DEPs from the spleens of chickens infected by ALV-J were detected. To find a relatively stable biomarker molecule, we summarized the DEPs at two timepoints and selected activating signal cointegrator 1 complex subunit 3 (ASCC3), TBC1 domain family member 2 (TBC1D2), MHC class II beta chain 1 (BLB2), ensconsin (MAP7), complement component 1 Q subcomponent B chain (C1QB), and Follistatin-like 1 (FSTL1) from both comparisons for protein interaction network analysis. ASCC3, BLB2, C1QB, and FSTL1 were potential biomarkers for the complex infection mechanism of ALV-J and the dynamic immune mechanism of the body.Entities:
Keywords: ALV-J; ASCC3; BLB2; C1QB; FSTL1; Proteomic
Year: 2019 PMID: 31475084 PMCID: PMC6702595 DOI: 10.1007/s13205-019-1863-9
Source DB: PubMed Journal: 3 Biotech ISSN: 2190-5738 Impact factor: 2.406