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dc.contributor.authorLu, HK
dc.contributor.authorMitchell, A
dc.contributor.authorEndoh, Y
dc.contributor.authorHampartzoumian, T
dc.contributor.authorHuynh, O
dc.contributor.authorBorges, L
dc.contributor.authorGeczy, C
dc.contributor.authorBryant, K
dc.contributor.authorTedla, N
dc.date.accessioned2020-12-22T05:51:34Z
dc.date.available2020-12-22T05:51:34Z
dc.date.issued2012
dc.identifierpii: PONE-D-11-14231
dc.identifier.citationLu, H. K., Mitchell, A., Endoh, Y., Hampartzoumian, T., Huynh, O., Borges, L., Geczy, C., Bryant, K. & Tedla, N. (2012). LILRA2 selectively modulates LPS-mediated cytokine production and inhibits phagocytosis by monocytes.. PLoS One, 7 (3), pp.e33478-. https://doi.org/10.1371/journal.pone.0033478.
dc.identifier.issn1932-6203
dc.identifier.urihttp://hdl.handle.net/11343/258371
dc.description.abstractThe activating immunoglobulin-like receptor, subfamily A, member 2 (LILRA2) is primarily expressed on the surface of cells of the innate immunity including monocytes, macrophages, neutrophils, basophils and eosinophils but not on lymphocytes and NK cells. LILRA2 cross-linking on monocytes induces pro-inflammatory cytokines while inhibiting dendritic cell differentiation and antigen presentation. A similar activating receptor, LILRA4, has been shown to modulate functions of TLR7/9 in dendritic cells. These suggest a selective immune regulatory role for LILRAs during innate immune responses. However, whether LILRA2 has functions distinct from other receptors of the innate immunity including Toll-like receptor (TLR) 4 and FcγRI remains unknown. Moreover, the effects of LILRA2 on TLR4 and FcγRI-mediated monocyte functions are not elucidated. Here, we show activation of monocytes via LILRA2 cross-linking selectively increased GM-CSF production but failed to induce IL-12 and MCP-1 production that were strongly up-regulated by LPS, suggesting functions distinct from TLR4. Interestingly, LILRA2 cross-linking on monocytes induced similar amounts of IL-6, IL-8, G-CSF and MIP-1α but lower levels of TNFα, IL-1β, IL-10 and IFNγ compared to those stimulated with LPS. Furthermore, cross-linking of LILRA2 on monocytes significantly decreased phagocytosis of IgG-coated micro-beads and serum opsonized Escherichia coli but had limited effect on phagocytosis of non-opsonized bacteria. Simultaneous co-stimulation of monocytes through LILRA2 and LPS or sequential activation of monocytes through LILRA2 followed by LPS led lower levels of TNFα, IL-1β and IL-12 production compared to LPS alone, but had additive effect on levels of IL-10 and IFNγ but not on IL-6. Interestingly, LILRA2 cross-linking on monocytes caused significant inhibition of TLR4 mRNA and protein, suggesting LILRA2-mediated suppression of LPS responses might be partly via regulation of this receptor. Taken together, we provide evidence that LILRA2-mediated activation of monocytes is significantly different to LPS and that LILRA2 selectively modulates LPS-mediated monocyte activation and FcγRI-dependent phagocytosis.
dc.languageeng
dc.publisherPublic Library of Science (PLoS)
dc.rights.urihttps://creativecommons.org/licenses/by/4.0
dc.titleLILRA2 selectively modulates LPS-mediated cytokine production and inhibits phagocytosis by monocytes.
dc.typeJournal Article
dc.identifier.doi10.1371/journal.pone.0033478
melbourne.affiliation.departmentDoherty Institute
melbourne.source.titlePLoS One
melbourne.source.volume7
melbourne.source.issue3
melbourne.source.pagese33478-
dc.rights.licenseCC BY
melbourne.elementsid1195990
melbourne.openaccess.pmchttp://www.ncbi.nlm.nih.gov/pmc/articles/PMC3316576
melbourne.contributor.authorLU, HAO
dc.identifier.eissn1932-6203
melbourne.accessrightsOpen Access


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