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...
Saved in:
Published in | The Journal of immunology (1950) Vol. 194; no. 1_Supplement; pp. 146 - 146.3 |
---|---|
Main Authors | , |
Format | Journal Article |
Language | English |
Published |
01.05.2015
|
Online Access | Get full text |
Cover
Loading…
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 |