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Cross reactive cellular immune responses in chickens previously exposed to low pathogenic avian influenza
BACKGROUND: Avian influenza (AI) infection in poultry can result in high morbidity and mortality, and negatively affect international trade. Because most AI vaccines used for poultry are inactivated, our knowledge of immunity against AI is based largely on humoral immune responses. In fact, little i...
Autores principales: | , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
BioMed Central
2011
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3108207/ https://www.ncbi.nlm.nih.gov/pubmed/21645292 http://dx.doi.org/10.1186/1753-6561-5-S4-S13 |
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author | Kapczynski, Darrell R Liljebjelke, Karen Kulkarni, Gururaj Hunt, Henry Jiang, Hai Jun Petkov, Daniel |
author_facet | Kapczynski, Darrell R Liljebjelke, Karen Kulkarni, Gururaj Hunt, Henry Jiang, Hai Jun Petkov, Daniel |
author_sort | Kapczynski, Darrell R |
collection | PubMed |
description | BACKGROUND: Avian influenza (AI) infection in poultry can result in high morbidity and mortality, and negatively affect international trade. Because most AI vaccines used for poultry are inactivated, our knowledge of immunity against AI is based largely on humoral immune responses. In fact, little is known about cellular immunity following a primary AI infection in poultry, especially regarding cytotoxic T lymphocytes (CTL’s). METHODS: In these studies, major histocompatibility complex (MHC)-defined (B(2)/B(2)) chickens were infected with low pathogenic AI (LPAI) H9N2 and clinical signs of disease were monitored over a two weeks period. Splenic lymphocytes from infected and naïve birds were examined for cross reactivity against homologous and heterologous (H7N2) LPAI by ex vivo stimulation. Cellular immunity was determined by cytotoxic lysis of B(2)/B(2) infected lung target cells and proliferation of T cells following exposure to LPAI. RESULTS: Infection with H9N2 resulted in statistically significant weight loss compared to sham-infected birds. Splenic lymphocytes derived from H9N2-infected birds displayed lysis of both homologous (H9N2) and heterologous (H7N2) infected target cells, whereas lymphocytes obtained from sham-infected birds did not. T cell proliferation was determined to be highest when exposed to the homologous virus. CONCLUSIONS: Taken together these data extend the findings that cellular immunity, including CTL’s, is cross reactive against heterologous isolates of AI and contribute to protection following infection. |
format | Online Article Text |
id | pubmed-3108207 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2011 |
publisher | BioMed Central |
record_format | MEDLINE/PubMed |
spelling | pubmed-31082072011-06-07 Cross reactive cellular immune responses in chickens previously exposed to low pathogenic avian influenza Kapczynski, Darrell R Liljebjelke, Karen Kulkarni, Gururaj Hunt, Henry Jiang, Hai Jun Petkov, Daniel BMC Proc Proceedings BACKGROUND: Avian influenza (AI) infection in poultry can result in high morbidity and mortality, and negatively affect international trade. Because most AI vaccines used for poultry are inactivated, our knowledge of immunity against AI is based largely on humoral immune responses. In fact, little is known about cellular immunity following a primary AI infection in poultry, especially regarding cytotoxic T lymphocytes (CTL’s). METHODS: In these studies, major histocompatibility complex (MHC)-defined (B(2)/B(2)) chickens were infected with low pathogenic AI (LPAI) H9N2 and clinical signs of disease were monitored over a two weeks period. Splenic lymphocytes from infected and naïve birds were examined for cross reactivity against homologous and heterologous (H7N2) LPAI by ex vivo stimulation. Cellular immunity was determined by cytotoxic lysis of B(2)/B(2) infected lung target cells and proliferation of T cells following exposure to LPAI. RESULTS: Infection with H9N2 resulted in statistically significant weight loss compared to sham-infected birds. Splenic lymphocytes derived from H9N2-infected birds displayed lysis of both homologous (H9N2) and heterologous (H7N2) infected target cells, whereas lymphocytes obtained from sham-infected birds did not. T cell proliferation was determined to be highest when exposed to the homologous virus. CONCLUSIONS: Taken together these data extend the findings that cellular immunity, including CTL’s, is cross reactive against heterologous isolates of AI and contribute to protection following infection. BioMed Central 2011-06-03 /pmc/articles/PMC3108207/ /pubmed/21645292 http://dx.doi.org/10.1186/1753-6561-5-S4-S13 Text en Copyright ©2011 Kapczynski et al; licensee BioMed Central Ltd. http://creativecommons.org/licenses/by/2.0 This is an open access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. |
spellingShingle | Proceedings Kapczynski, Darrell R Liljebjelke, Karen Kulkarni, Gururaj Hunt, Henry Jiang, Hai Jun Petkov, Daniel Cross reactive cellular immune responses in chickens previously exposed to low pathogenic avian influenza |
title | Cross reactive cellular immune responses in chickens previously exposed to low pathogenic avian influenza |
title_full | Cross reactive cellular immune responses in chickens previously exposed to low pathogenic avian influenza |
title_fullStr | Cross reactive cellular immune responses in chickens previously exposed to low pathogenic avian influenza |
title_full_unstemmed | Cross reactive cellular immune responses in chickens previously exposed to low pathogenic avian influenza |
title_short | Cross reactive cellular immune responses in chickens previously exposed to low pathogenic avian influenza |
title_sort | cross reactive cellular immune responses in chickens previously exposed to low pathogenic avian influenza |
topic | Proceedings |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3108207/ https://www.ncbi.nlm.nih.gov/pubmed/21645292 http://dx.doi.org/10.1186/1753-6561-5-S4-S13 |
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