The expression of mouse CLEC‐2 on leucocyte subsets varies according to their anatomical location and inflammatory state
Identifieur interne : 001722 ( Main/Exploration ); précédent : 001721; suivant : 001723The expression of mouse CLEC‐2 on leucocyte subsets varies according to their anatomical location and inflammatory state
Auteurs : Kate L. Lowe ; Leyre Navarro-Nú Ez ; Cécile Bénézech ; Saba Nayar ; Bethany L. Kingston ; Bernhard Nieswandt ; Francesca Barone ; Steve P. Watson ; Christopher D. Buckley ; Guillaume E. DesantiSource :
- European Journal of Immunology [ 0014-2980 ] ; 2015.
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
Url:
DOI: 10.1002/eji.201445314
PubMed: 26173808
PubMed Central: 4737233
Affiliations:
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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<sup>high</sup> Gr‐1<sup>high</sup> myeloid cells lose CLEC‐2 following entry into secondary lymphoid organs. 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