2. MHV receptor
In collaboration with K.V. Holmes (Denver, USA), expression of CEACAM1, a glycoprotein that serves as receptor for MHV-A59 has been analysed in cells from the immune system (11). This molecule was highly expressed in B lymphocytes, including cells of the B-1a (CD5+) lineage, and in macrophages, but was not detectable in resting T lymphocytes. Bgp1a is also expressed in endothelial and thymic epithelial cells. Thus, some alterations of immune responses induced by MHV might be explained by the expression of the viral receptor on immune cells. For instance, MHV-A59 infection of adult BALB/c mice induces a severe, transient atrophy of the thymus that may result from apoptosis of immature double-positive T cells resulting from infection of a small proportion of thymus epithelial cells (12).
CEACAM1 was also found to be expressed on a minority of mouse natural killer (NK) cells, especially in the liver (13). CEACAM1 expression on NK cells depended on their differentiation stage, with highest levels on immature CD49b- NK cells. Expression of CEACAM1 on NK cells was strongly enhanced by in vitro activation with IL-12 and IL-18. However, in vivo NK cell stimulation by infection with LDV did not lead to strong CEACAM1 expression, even on activated interferon-gamma-producing NK cells. These results indicate that CEACAM1 expression is differently regulated, depending on NK cell activation pathway, which may lead to distinct regulatory mechanisms of functional subpopulations of these cells.
To know more... (pdf chapter of the last de Duve Institute report)
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