This procedure involved by active immunity of birds when expose to NDV infection.
Mechanism of Action
As soon as 6 hours after exposure, splenic cells produce alpha and beta interferon, and interleukin 6 (IL-6) when exposed to vNDV, but not to loNDV.
Interferon gamma (IFN-γ) secreted from NK cells activates macrophages and promotes cell-mediated immunity (CMI) 1 day after infection.
Whole chicken genome arrays of the host immune response to NDV at 1–2 days after infection demonstrate the induction of type I and II interferons, cytokines, chemokines, and inducible nitric oxide synthase.
Upon infection, chicken embryo fibroblasts produce interferon alpha but little to no interferon beta. The innate immune response alone is not enough to ensure survival of the host after an exposure to a vNDV.
However, the activity of NK cells, which are able to destroy virus-infected cells, improves as chickens age and this improvement could provide some explanation for decreased susceptibility with older birds.
Once the virus overcomes the innate immune response, cellular and humoral responses are initiated by the host.
T-lymphocyte differentiation occurs in the thymus gland, producing cells able to rapidly expand after being exposed to the antigen a second time, providing CMI that is measured by lymphocyte proliferation or cytokine secretion .
Cytotoxic T lymphocytes (CD8) are found in splenic cells of chickens twice infected with NDV. Cell-mediated immunity of a T helper cell type 1 (Th1) response, characterized by the production of IFN-γ by macrophages, can be detected 3 days after infection with a live NDV vaccine strains, thus providing signals for a humoral response to develop by the host.
Macrophages also induce nitric oxide (NO) production and the amount of NO produced is elevated in birds with higher antibody levels, demonstrating how CMI and humoral immunity affect each other. Similar to innate immunity,
CMI alone is not enough to ensure survival of the host after an exposure to a vNDV. However, IFN-γ produced in large quantities at the same time as the vNDV is replicating in the host significantly reduces mortality and moderately reduced morbidity, providing evidence of the role of CMI in NDV infection). This also underscores the need for humoral immunity
After exposure to NDV, B-lymphocytes differentiate into plasma cells that secrete 3 types of neutralizing antibodies specific to the antigen . These antibodies are necessary to protect birds from morbidity and mortality after infection with vNDV.
First, IgM is produced and can be detected as early as 4 days after vaccination .
After 7 days, IgG (referred to as IgY in birds due to a structural difference) and IgA, which is important to the local immunity of the Harderian gland and cecal tonsils, can be detected.
At 7 days postinfection the splenic tissue is comprised of 56% IgM, 37% IgY and 7% IgA. Again, evidence for the intertwining of CMI and humoral immunity is demonstrated with IL-4 secretion, improving the humoral immune response.
Local immunity is evaluated by the amount of antigen-specific IgA antibodies that can be detected in tears, tracheal washings, and bile after intranasal or intraocular exposure to live NDV vaccines. Local immunity (IgA) is important in neutralizing free virions in the respiratory and gastrointestinal tracts
Ref: Diseases of poultry, 13th edition, Poultry disease. 6th edition