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Abstract
Expression of mouse C-type lectin-like receptor 2 (CLEC-2) has been reported on circulating CD11bhigh Gr-1high 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 CD11bhigh Gr-1high 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 language | English |
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Pages (from-to) | 2484–2493 |
Journal | European Journal of Immunology |
Volume | 45 |
Issue number | 9 |
Early online date | 12 Aug 2015 |
DOIs | |
Publication status | Published - 7 Sept 2015 |
Keywords
- CLEC-2
- Inflammation
- Leucocytes
- Mouse
- Tamoxifen
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