Abstract
BackgroundThe pathogenesis of immunological tolerance caused by avian leukosis virus subgroup J (ALV-J), an oncogenic retrovirus, is largely unknown.ResultsIn this study, the development, differentiation, and immunological capability of B cells and their progenitors infected with ALV-J were studied both morphologically and functionally by using a model of ALV-J congenital infection. Compared with posthatch infection, congenital infection of ALV-J resulted in severe immunological tolerance, which was identified as the absence of detectable specific antivirus antibodies. In congenitally infected chickens, immune organs, particularly the bursa of Fabricius, were poorly developed. Moreover, IgM-and IgG-positive cells and total immunoglobulin levels were significantly decreased in these chickens. Large numbers of bursa follicles with no differentiation into cortex and medulla indicated that B cell development was arrested at the early stage. Flow cytometry analysis further confirmed that ALV-J blocked the differentiation of CD117+chB6+ B cell progenitors in the bursa of Fabricius. Furthermore, both the humoral immunity and the immunological capability of B cells and their progenitors were significantly suppressed, as assessed by (a) the antibody titres against sheep red blood cells and the Marek’s disease virus attenuated serotype 1 vaccine; (b) the proliferative response of B cells against thymus-independent antigen lipopolysaccharide (LPS) in the spleen germinal centres; and (c) the capacities for proliferation, differentiation and immunoglobulin gene class-switch recombination of B cell progenitors in response to LPS and interleukin-4(IL-4) in vitro.ConclusionsThese findings suggested that the anergy of B cells in congenitally infected chickens is caused by the developmental arrest and dysfunction of B cell progenitors, which is an important factor for the immunological tolerance induced by ALV-J.
Highlights
Avian leukosis virus subgroup J (ALV-J), an oncogenic retrovirus, causes myeloid leukosis and various other neoplastic diseases in both broiler and layer chickens [1, 2]
Chickens infected at ED 6 suffered immunological tolerance and showed development arrest of bursal follicles and B cells Consistent with previous studies [6, 28, 29], current ELISA test results showed that chickens infected at day 6 of embryogenesis (ED 6) had high levels of specific p27 antigen of avian leukosis virus subgroup J (ALV-J) but no detectable anti-ALV-J antibody in vivo
The results suggested that all experimental chickens infected with ALV-J at ED 6 have developed immunological tolerance
Summary
Avian leukosis virus subgroup J (ALV-J), an oncogenic retrovirus, causes myeloid leukosis and various other neoplastic diseases in both broiler and layer chickens [1, 2]. Previous studies have suggested the presence of lymphocyte depletion in special areas of immune organs and the unusual expression of cytokine genes associated with immunity in chickens that are inoculated with ALV-J after hatching [11,12,13]. These data indicated that ALV-J has selective effects on lymphocyte type and development stage. The pathogenesis of immunological tolerance caused by avian leukosis virus subgroup J (ALV-J), an oncogenic retrovirus, is largely unknown
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