Alterations in MHCII expression on B cells isolated from cattle naturally infected with bovine leukemia virus. (VET1P.1115)

Abstract Bovine leukemia virus (BLV) is a deltaretrovirus that infects B cells and is widespread in US dairy herds. 83% of US dairy herds are infected with BLV and the within-herd infection burden is estimated to be as high as 46%. BLV infection causes reduced milk production and decreased longevity...

Full description

Saved in:
Bibliographic Details
Published inThe Journal of immunology (1950) Vol. 194; no. 1_Supplement; pp. 146 - 146.3
Main Authors Frie, Meredith, Coussens, Paul
Format Journal Article
LanguageEnglish
Published 01.05.2015
Online AccessGet full text

Cover

Loading…
More Information
Summary:Abstract Bovine leukemia virus (BLV) is a deltaretrovirus that infects B cells and is widespread in US dairy herds. 83% of US dairy herds are infected with BLV and the within-herd infection burden is estimated to be as high as 46%. BLV infection causes reduced milk production and decreased longevity, which leads to economic losses of $520 million every year. However, BLV is predicted to cause immune suppression in infected cattle, which would increase the economic losses incurred as a result of BLV infection in dairy cattle. To characterize cellular mechanisms of immune suppression in BLV-infected cattle, the expression of MHCII in B cells from naturally infected dairy cattle was investigated. PBMCs were isolated from healthy dairy cattle or naturally infected dairy cattle and the MHCII expression on B cells was assessed in unstimulated or pokeweed mitogen-stimulated culture conditions. qRT-PCR and flow cytometry were used to determine the change in MHCII expression on B cells isolated from BLV-infected cattle. BLV-infected cattle have a significantly higher mean relative percentage of B cells expressing MHCII, but significantly reduced mean fluorescence intensity of MHCII. This could suggest that B cells from BLV-infected cattle are less efficient at presenting peptide antigens to CD4+ T cells.
ISSN:0022-1767
1550-6606
DOI:10.4049/jimmunol.194.Supp.146.3