2014
DOI: 10.1002/eji.201444593
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To the Editor Murine gammaherpesvirus 68 (MHV‐68) escapes from NK‐cell‐mediated immune surveillance by a CEACAM1‐mediated immune evasion mechanism

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Cited by 7 publications
(6 citation statements)
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“…Because KS is a highly angiogenic tumor, we wanted to investigate the induction of CEACAM1 expression by vIL-6. Furthermore, CEACAM1 and a CEACAM1 homolog have been shown to contribute to the pathogenesis of other herpesviruses, but the role of CEACAM1 during KSHV infection has not yet been investigated ( 47 , 66 , 67 ).…”
Section: Discussionmentioning
confidence: 99%
See 1 more Smart Citation
“…Because KS is a highly angiogenic tumor, we wanted to investigate the induction of CEACAM1 expression by vIL-6. Furthermore, CEACAM1 and a CEACAM1 homolog have been shown to contribute to the pathogenesis of other herpesviruses, but the role of CEACAM1 during KSHV infection has not yet been investigated ( 47 , 66 , 67 ).…”
Section: Discussionmentioning
confidence: 99%
“…Previous microarray studies of immortalized dermal microvascular endothelial cells infected with KSHV also reported that the gene for CEACAM1 was one of multiple genes affected by KSHV infection ( 69 ). Furthermore, CEACAM1 was found to be upregulated in the lungs of mice infected with the murine gammaherpesvirus MHV68 ( 66 , 67 ). In the present study, we found that both KSHV latent and de novo infection of endothelial cells upregulated CEACAM1 expression compared to that in uninfected cells, and reactivation of PEL also resulted in increased CEACAM1 expression.…”
Section: Discussionmentioning
confidence: 99%
“…The murine gammaherpesvirus MHV-68 upregulates the inhibitory receptor carcinoembryonic antigen-related cell adhesion molecule 1 (CEACAM1) on alveolar epithelial cells, and there are indications that this upregulation, via homophilic trans interactions with CEACAM1 on NK cells, may result in suppressed NK cell activity (122).…”
Section: Herpesvirus Nk Cell Evasion Strategiesmentioning
confidence: 99%
“…Among those are SIRPα and CEACAM1 and CEACAM3, members of the human carcinoembryonic antigen-related cell-cell adhesion molecule (CEACAM) family which have inhibitory ITIM/ ITSM motifs and activating ITAM-like motifs in their cytoplasmic regions, respectively [3,4]. A number of bacterial pathogens like pathogenic Neisseria (N. gonorrhoeae, N. meningitis) Haemophilus influenzae and Moraxella catarrhalis have been shown to bind to the N-terminal immunoglobulin (Ig) variable-like domain of CEACAM1 on epithelial and immune cells allowing both entry into the host by transcytosis and downregulation of the host's immune response by inhibiting adaptive and innate immune reactions [5][6][7][8][9][10][11]. Pathogens thus exploit the normal physiological function of CEA-CAM1 which acts as an immune inhibitory receptor on leukocytes upon homotypic or heterotypic interactions for example with other CEACAM members [7,12].…”
Section: Introductionmentioning
confidence: 99%