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.

Original publication




Journal article


Eur J Immunol

Publication Date





2484 - 2493


CLEC-2, Inflammation, Leucocytes, Mouse, Tamoxifen, Animals, Antibodies, Monoclonal, B-Lymphocytes, Blood Platelets, CD11b Antigen, Cell Movement, Dendritic Cells, Gene Expression Regulation, Inflammation, Lectins, C-Type, Lipopolysaccharides, Lymph Nodes, Mice, Mice, Transgenic, Myeloid Cells, Organ Specificity, Receptors, Chemokine, Signal Transduction, Spleen