Systems of antigen delivery into antigen-presenting cells represent an important novel strategy in chicken vaccine development. In this study, we verified the ability of Rous sarcoma virus (RSV) antigens fused with streptavidin to be targeted by specific biotinylated monoclonal antibody (anti-CD205) into dendritic cells and induce virus-specific protective immunity. The method was tested in four congenic lines of chickens that are either resistant or susceptible to the progressive growth of RSV-induced tumors. Our analyses confirmed that the biot-anti-CD205-SA-FITC complex was internalized by chicken splenocytes. In the cytokine expression profile, several significant differences were evident between RSV-challenged progressor and regressor chicken lines. A significant up-regulation of IL-2, IL-12, IL-15, and IL-18 expression was detected in immunized chickens of both regressor and progressor groups. Of these cytokines, IL-2 and IL-12 were most up-regulated 14 days post-challenge (dpc), while IL-15 and IL-18 were most up-regulated at 28 dpc. On the contrary, IL-10 expression was significantly down-regulated in all immunized groups of progressor chickens at 14 dpc. We detected significant up-regulation of IL-17 in the group of immunized progressors. LITAF down-regulation with iNOS up-regulation was especially observed in the progressor group of immunized chickens that developed large tumors. Based on the increased expression of cytokines specific for activated dendritic cells, we conclude that our system is able to induce partial stimulation of specific cell types involved in cell-mediated immunity.

• MeSH
• Antigens, Viral immunology   MeSH
• Immunity, Cellular immunology   MeSH
• Antigens, CD immunology   MeSH
• Cytokines physiology   MeSH
• Dendritic Cells immunology   virology   MeSH
• Chickens immunology   virology   MeSH
• Lectins, C-Type immunology   MeSH
• Antibodies, Bispecific immunology   MeSH
• Sarcoma, Avian immunology   prevention & control   MeSH
• Receptors, Cell Surface immunology   MeSH
• Minor Histocompatibility Antigens immunology   MeSH
• Viral Vaccines immunology   MeSH
• Rous sarcoma virus immunology   MeSH
• Animals, Congenic immunology   virology   MeSH
• Animals MeSH
• Check Tag
• Animals MeSH
• Publication type
• Journal Article MeSH
• Research Support, Non-U.S. Gov't MeSH
• Names of Substances
• Antigens, Viral MeSH
• Antigens, CD MeSH
• Cytokines MeSH
• DEC-205 receptor MeSH Browser
• Lectins, C-Type MeSH
• Antibodies, Bispecific MeSH
• Receptors, Cell Surface MeSH
• Minor Histocompatibility Antigens MeSH
• Viral Vaccines MeSH

The growth pattern (progression/regression) of v-src DNA- and Rous sarcoma virus (RSV)-induced tumors was analogous on a panel of inbred chicken lines. The decisive role of the major histocompatibility complex [Mhc(B)] alleles in resistance to the progression of these tumors was formally proved in segregating backcross populations. The immune mechanism of tumor regression was demonstrated by both in vivo and in vitro assays. A protective effect of v-src-specific immunity against RSV challenge was shown in Rous sarcoma regressor, line CB (B12/B12). Immune cells from regressors of v-src DNA-induced tumors can protect syngeneic hosts from the development of tumor after challenge with both v-src DNA and RSV. Suppression of RSV-induced tumor cell growth in vitro was also achieved by the use of cocultivation with spleen cells from chickens in which v-src DNA-induced tumors had regressed. This in vitro sarcoma-specific response was Mhc(B)-restricted. Chickens of the congenic Rous sarcoma progressor line CC (B4/B4) are sometimes able to regress v-src DNA-induced tumors, but immune cells can only slow the growth of v-src DNA-induced tumors in syngeneic hosts. This suggests that the primary reason for the susceptibility of CC chickens is a weak v-src-specific immune response. Furthermore, some of the v-src DNA-induced tumors were transplantable across the Mhc(B) barrier. The growth of tumor allografts was able to be facilitated when immunological tolerance to the B-F/L region antigens (class I and class II) had been established. This demonstrated that a high tumorigenicity of the transplantable tumor was not due to the lack of Mhc(B) antigens on tumor cells.

• MeSH
• DNA, Viral genetics   MeSH
• Neoplasms, Experimental immunology   MeSH
• Genes, src * MeSH
• Major Histocompatibility Complex * MeSH
• Inbreeding MeSH
• Chickens immunology   MeSH
• Oncogene Protein pp60(v-src) immunology   MeSH
• Repetitive Sequences, Nucleic Acid MeSH
• Cell Transformation, Viral MeSH
• Avian Sarcoma Viruses genetics   MeSH
• Animals MeSH
• Check Tag
• Male MeSH
• Female MeSH
• Animals MeSH
• Publication type
• Journal Article MeSH
• Research Support, Non-U.S. Gov't MeSH
• Names of Substances
• DNA, Viral MeSH
• Oncogene Protein pp60(v-src) MeSH