dPRLR causes differences in immune responses between early and late feathering chickens after ALV-J infection
0301 basic medicine
Receptors, Prolactin
Epidemiology
Veterinary medicine
Immunology
Transgene Expression
immune response
03 medical and health sciences
Endocrinology
Biochemistry, Genetics and Molecular Biology
SF600-1100
Health Sciences
dPRLR
Genetics
Animals
Biology
Internal medicine
Poultry Diseases
Antibody
Immunology and Microbiology
2. Zero hunger
0303 health sciences
Avian Leukosis Virus
early feathering chickens
FOS: Clinical medicine
Immunity
Life Sciences
Hormone
Prolactin
3. Good health
Herpesviruses: Epidemiology, Pathogenesis, and Management
Immune system
Avian Leukosis
Immunoglobulin M
Growth Hormone
Immunoglobulin G
FOS: Biological sciences
Medicine
ALV-J
Gene Therapy Techniques and Applications
Chickens
Spleen
late feathering chickens
Research Article
Natural Killer Cells in Immunity
DOI:
10.1186/s13567-021-01016-7
Publication Date:
2022-01-08T20:02:42Z
AUTHORS (12)
ABSTRACT
AbstractTo understand the differences in immune responses between early feathering (EF) and late feathering (LF) chickens after infection with avian leukosis virus, subgroup J (ALV-J), we monitored the levels of prolactin, growth hormone and the immunoglobulins IgG and IgM in the serum of LF and EF chickens for 8 weeks. Moreover, we analysed the expression of immune-related genes in the spleen and the expression of PRLR, SPEF2 and dPRLR in the immune organs and DF-1 cells by qRT–PCR. The results showed that ALV-J infection affected the expression of prolactin, growth hormone, IgG and IgM in the serum. Regardless of whether LF and EF chickens were infected with ALV-J, the serum levels of the two hormones and two immunoglobulins in EF chickens were higher than those in LF chickens (P < 0.05). However, the expression of immune-related genes in the spleen of positive LF chickens was higher than that in the spleen of positive EF chickens. In the four immune organs, PRLR and SPEF2 expression was also higher in LF chickens than in EF chickens. Furthermore, the dPRLR expression of positive LF chickens was higher than that of negative LF chickens. After infection with ALV-J, the expression of PRLR in DF-1 cells significantly increased. In addition, overexpression of PRLR or dPRLR in DF-1 cells promoted replication of ALV-J. These results suggested that the susceptibility of LF chickens to ALV-J might be induced by dPRLR.
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