MHC Expression on Spleen Lymphocyte Subsets in Genetically Resistant and Susceptible Chickens Infected with Marek's Disease Virus

Tina Dalgaard, Mette K. Bøving, Kurt Handberg, Karin H. Jensen, Liselotte R. Norup, Helle R. Juul-Madsen

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    Abstract

    Resistance and susceptibility to Marek's disease (MD) are strongly influenced by the chicken major histocompatibility complex (MHC). In this study, splenic lymphocytes from MD-resistant and MD-susceptible chickens of three MHC genotypes (B21/B21, B19/B21, and B19/B19) were analyzed by flow cytometry for MHC surface expression. In the spleen, constitutive MHC class I surface expression was found to be highest in homozygous B19, lowest in homozygous B21, and intermediate in heterozygous B19/B21 animals. This was observed on CD4(+), CD8(+), and Bu-1(+) splenic lymphocytes. Chickens of all three genotypes were subjected to infection with MD virus (GA strain) and spleen samples from infected as well as MHC-matched negative controls were analyzed at 1, 4, and 8 wk post-infection (p.i.). It was observed that MDV induced an increase in MHC class I expression late in the infection. Thus, MHC class I was increased on the surface of CD4(+) cells from infected chickens of all genotypes at 4 and 8 wk p.i. compared with negative controls. Also, MHC class I expression was increased on CD8(+) cells from infected chickens of all genotypes at 4 and 8 wk p.i., except for the homozygous B19 animals, that showed no increase at 8 wk p.i. MDV-induced differences in MHC class II surface levels were also found. Thus, MHC class II expression was increased on CD4(+) cells from infected B19/21 and B21/B21 chickens at 4 wk p.i., and also at 8 wk p.i. on CD4(+) cells from infected B19/B21 animals. MHC class II expression was increased on CD8(+) cells from infected chickens of all genotypes at 4 wk p.i. These findings suggest that MDV infection in vivo increases the level of MHC surface expression on splenic T cells, indicating a possible role in immunity against MDV.
    Original languageEnglish
    JournalViral Immunology
    Volume22
    Issue number5
    Pages (from-to)321-327
    ISSN0882-8245
    DOIs
    Publication statusPublished - 2009

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