Background:The biological function of a former orphan receptor, GPR84, has not been clarified yet. Results: GPR84 activation results in chemotaxis and cytokine production by the stimulation of potential ligands and the surrogate agonist. Conclusion: GPR84 works as a proinflammatory receptor in myeloid cells. Significance: This study provides new insights into the function of GPR84.
The Us3 kinase is part of the antiapoptotic arsenal that salvages herpes simplex virus (HSV)-1-infected cells from damage caused by different stimuli. We demonstrate that Us3 protects HSV-1-infected cells from lysis by MHC class Irestricted CD8T cells without affecting antigen presentation. Expression of Us3 was associated with inhibition of caspase activation and reduced cleavage of the proapoptotic protein Bid. Recombinant granzyme B (GrB) failed to cleave Bid in cytosolic extracts from Us3 positive cells, while recombinant Bid served as substrate for Us3 phosphorylation, suggesting that modification of Bid by Us3 blocks its processing by GrB. Our data illustrate a new strategy of viral escape, where modification of a cellular proapoptotic substrate may prevent lysis of the infected cells without affecting other T-cell functions.
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