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Eur J Immunol. 2015 Sep;45(9):2484-93. doi: 10.1002/eji.201445314. Epub 2015 Aug 12.

The expression of mouse CLEC-2 on leucocyte subsets varies according to their anatomical location and inflammatory state.

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Centre for Cardiovascular Sciences, University of Birmingham, Birmingham, UK.
MRC Centre for Immune Regulation, University of Birmingham, Birmingham, UK.
Centre for Translational Inflammation Research, Rheumatology Research Group, University of Birmingham, Birmingham, UK.
Medical School, University of Oxford, Oxford, UK.
Department of Experimental Biomedicine, University Hospital, University of Würzburg, Würzburg, Germany.


Expression of mouse C-type lectin-like receptor 2 (CLEC-2) has been reported on circulating CD11b(high) Gr-1(high) myeloid cells and dendritic cells (DCs) under basal conditions, as well as on a variety of leucocyte subsets following inflammatory stimuli or in vitro cell culture. However, previous studies assessing CLEC-2 expression failed to use CLEC-2-deficient mice as negative controls and instead relied heavily on single antibody clones. Here, we generated CLEC-2-deficient adult mice using two independent approaches and employed two anti-mouse CLEC-2 antibody clones to investigate surface expression on hematopoietic cells from peripheral blood and secondary lymphoid organs. We rule out constitutive CLEC-2 expression on resting DCs and show that CLEC-2 is upregulated in response to LPS-induced systemic inflammation in a small subset of activated DCs isolated from the mesenteric lymph nodes but not the spleen. Moreover, we demonstrate for the first time that peripheral blood B lymphocytes present exogenously derived CLEC-2 and suggest that both circulating B lymphocytes and CD11b(high) Gr-1(high) myeloid cells lose CLEC-2 following entry into secondary lymphoid organs. These results have significant implications for our understanding of CLEC-2 physiological functions.


CLEC-2; Inflammation; Leucocytes; Mouse; Tamoxifen

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