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Your search keyword '"Brown, Gordon D."' showing total 17 results
Start Over Author "Brown, Gordon D." Journal european journal of immunology
17 results on '"Brown, Gordon D."'

5. Mycobacterial receptor, Clec4d (CLECSF8, MCL), is coregulated with Mincle and upregulated on mouse myeloid cells following microbial challenge.

Author

Kerscher, Bernhard, Wilson, Gillian J., Reid, Delyth M., Mori, Daiki, Taylor, Julie A., Besra, Gurdyal S., Yamasaki, Sho, Willment, Janet A., and Brown, Gordon D.

Abstract

The C-type lectin receptor (CTLR), Clec4d (MCL, CLECSF8), is a member of the Dectin-2 cluster of CTLRs, which also includes the related receptors Mincle and Dectin-2. Like Mincle, Clec4d recognizes mycobacterial cord factor, trehalose dimycolate, and we recently demonstrated its key role in anti-mycobacterial immunity in mouse and man. Here, we characterized receptor expression in naïve mice, under inflammatory conditions, and during Mycobacterium bovis BCG infection using newly generated monoclonal antibodies. In naïve mice, Clec4d was predominantly expressed on myeloid cells within the peritoneal cavity, blood, and bone marrow. Unexpectedly, basal expression of Clec4d was very low on leukocytes in the lung. However, receptor expression was significantly upregulated on pulmonary myeloid cells during M. bovis BCG infection. Moreover, Clec4d expression could be strongly induced in vitro and in vivo by various microbial stimuli, including TLR agonists, but not exogenous cytokines. Notably, we show that Clec4d requires association with the signaling adaptor FcRγ and Mincle, but not Dectin-2, for surface expression. In addition, we provide evidence that Clec4d and Mincle, but not Dectin-2, are interdependently coregulated during inflammation and infection. These data show that Clec4d is an inducible myeloid-expressed CTLR in mice, whose expression is tightly linked to that of Mincle. [ABSTRACT FROM AUTHOR]

Published
2016
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9. Syk kinase is required for collaborative cytokine production induced through Dectin-1 and Toll-like receptors

Author

Dennehy, Kevin M., primary, Ferwerda, Gerben, additional, Faro-Trindade, Inês, additional, Pyż, Elwira, additional, Willment, Janet A., additional, Taylor, Philip R., additional, Kerrigan, Ann, additional, Tsoni, S. Vicky, additional, Gordon, Siamon, additional, Meyer-Wentrup, Friederike, additional, Adema, Gosse J., additional, Kullberg, Bart-Jan, additional, Schweighoffer, Edina, additional, Tybulewicz, Victor, additional, Mora-Montes, Hector M., additional, Gow, Neil A. R., additional, Williams, David L., additional, Netea, Mihai G., additional, and Brown, Gordon D., additional

Published
2008
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17. The human beta-glucan receptor is widely expressed and functionally equivalent to murine Dectin-1 on primary cells.

Author

Willment JA, Marshall AS, Reid DM, Williams DL, Wong SY, Gordon S, and Brown GD

Subjects
Animals, Antibodies, Monoclonal, Dendritic Cells immunology, Dendritic Cells metabolism, Eosinophils immunology, Eosinophils metabolism, Flow Cytometry, Humans, Lectins, C-Type, Macrophages immunology, Membrane Proteins immunology, Mice, Nerve Tissue Proteins immunology, Neutrophils immunology, Neutrophils metabolism, Receptors, Immunologic immunology, Species Specificity, Macrophages metabolism, Membrane Proteins metabolism, Nerve Tissue Proteins metabolism, Receptors, Immunologic metabolism
Abstract

We identified the C-type-lectin-like receptor, Dectin-1, as the major receptor for fungal beta-glucans on murine macrophages and have demonstrated that it plays a significant role in the cellular response to these carbohydrates. Using two novel, isoform-specific mAb, we show here that human Dectin-1, the beta-glucan receptor (betaGR), is widely expressed and present on all monocyte populations as well as macrophages, DC, neutrophils and eosinophils. This receptor is also expressed on B cells and a subpopulation of T cells, demonstrating that human Dectin-1 is not myeloid restricted. Both major functional betaGR isoforms - betaGR-A and betaGR-B - were expressed by these cell populations in peripheral blood; however, only betaGR-B was significantly expressed on mature monocyte-derived macrophages and immature DC, suggesting cell-specific control of isoform expression. Inflammatory cells, recruited in vivo using a new skin-window technique, demonstrated that Dectin-1 expression was not significantly modulated on macrophages during inflammation, but is decreased on recruited granulocytes. Despite previous reports detailing the involvement of other beta-glucan receptors on mature human macrophages, we have demonstrated that Dectin-1 acted as the major beta-glucan receptor on these cells and contributed to the inflammatory response to these carbohydrates.

Published
2005
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