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PKR Regulates Immunoglobulin Class Switching during RSV infection In Vivo
Author(s) -
Thakur Sheetal A.,
Zalinger Zachary,
Johnson Teresa R,
Corn Minor Radiah A.,
Graham Barney S,
Imani Farhad
Publication year - 2010
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.24.1_supplement.952.11
Subject(s) - protein kinase r , antibody , immunoglobulin e , virus , biology , humoral immunity , virology , immune system , immunology , immunoglobulin g , eif 2 kinase , western blot , immunity , immunoglobulin class switching , protein kinase a , kinase , b cell , gene , mitogen activated protein kinase kinase , biochemistry , cyclin dependent kinase 2 , microbiology and biotechnology
Effective antibody responses play a critical role in protection against many pathogenic viruses including respiratory synctial virus (RSV). The humoral response during RSV infection is comprised of a combination of immunoglobulin (Ig) isotypes such as IgG, IgA and IgE. Previous studies from our laboratory have established protein kinase R (PKR) as an important mediator of RSV‐induced innate immunity and immunopathology. In this report the role of PKR in regulation of RSV induced Ig class switching in a mouse model was investigated. Wild type (WT) and PKR‐deficient (PKR −/− ) mice were infected with RSV intratracheally (10 7 pfu/mouse) and serum Ig levels were determined at 3, 7 and 14 days post‐infection. Increased serum levels of IgA, IgG and IgE were observed in WT mice compared to the PKR −/− mice. Furthermore, western blot analysis on extracts from RSV infected cells, showed that serum from infected WT mice contained significantly greater levels of RSV‐specific IgG and IgA than serum from PKR −/− mice. Several immunoregulatory cytokines including TGF‐[beta], IL‐6 and IFN‐[gamma] were significantly lower in PKR −/− mice compared to the WT mice. Taken together, these results demonstrate that PKR plays an important role in virus‐specific Ig responses.