| Abstrakt: |
We have shown that the ability of PECAM-1 & JAM-A to mediate leukocyte transmigration in vivo is stimulus-specific, eg both molecules mediate leukocyte transmigration through cremasteric venules of C57BL/6 mice as elicited by IL-1β but not TNFα. As it has been suggested that in contrast to some other laboratory mouse strains, C57BL/6 mice can compensate for PECAM-1 blockade/deletion (Schenkel et al., 2004), we sought to investigate whether the stimulus-specific roles of PECAM-1/JAM-A in the cremaster muscle model are governed by the strain of mice used. In line with the findings of Schenkel et al., the anti-PECAM-1 blocking mAb Mec 13.3 suppressed thioglycollate-induced leukocyte migration into the peritoneum of SJL but not C57BL/6 mice. In contrast, in the cremaster muscle model whilst IL-1β-induced leukocyte transmigration (as observed by IVM) was inhibited by Mec 13.3 in the mouse strains C57BL/6, FVB and SJL (84 %, 93% and 100% inhibition, respectively), no inhibition of TNFα-induced transmigration was noted in these mouse strains. In addition, the anti-JAM-A mAb BV-11, blocked IL-1β-induced, but not TNFα-induced, leukocyte transmigration in both C57BL/6 and FVB mice. The results suggest that the stimulus-specific roles of PECAM-1 & JAM-A in different mouse strains may be governed by the inflammatory model employed. [ABSTRACT FROM AUTHOR] |
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