Ubiquitous versus restricted expression of the two mouse dendritic cell C-type lectin receptors, DCIR1 and DCAR2, among myeloid cells.

Biochem Biophys Res Commun

Department of Integrated Biosciences, Graduate School of Frontier Sciences, The University of Tokyo, 5-1-5 Kashiwanoha, Kashiwa, Chiba, 277-8562, Japan. Electronic address:

Published: November 2015

AI Article Synopsis

  • DCIR1 and DCAR2 are mouse lectin receptors found on antigen presenting cells, with a high structural similarity in their C-type lectin domains.
  • Researchers developed specific antibodies that can clearly distinguish between DCIR1 and DCAR2, and examined their presence in different immune cells.
  • While DCIR1 is widely expressed in various myeloid cells, DCAR2 shows specific expression in certain cDC subpopulations, particularly in skin-draining lymph nodes, indicating its potential role as a marker for migratory cDCs.

Article Abstract

Dendritic cell inhibitory receptor 1 (DCIR1, also known as DCIR and Clec4a2) and dendritic cell activating receptor 2 (DCAR2, also known as DCAR and Clec4b1) are mouse lectin receptors expressed on antigen presenting cells. They have structurally similar C-type lectin domains, of which amino acid sequences show 90.5% identity, and commercially available antibodies against them cross-react each other. Here we have established novel antibodies against DCIR1 and DCAR2 that can unambiguously discriminate DCIR1 and DCAR2 and examined their distribution among various immune cells. While DCIR1 was ubiquitously expressed on myeloid cells, including conventional DCs (cDCs), macrophages, neutrophils and eosinophils, in various immune organs, significant expression of DCAR2 was detected only on subpopulations of cDCs from bone marrow and skin-draining lymph nodes. Interestingly, in FITC-painted mice, DCAR2 was expressed on all of the FITC(+) cDCs, which had migrated from the skin after FITC painting, suggesting that DCAR2 can be a marker of migratory cDCs in skin-draining lymph nodes. Our findings provide a basis to investigate in vivo function of DCIR1 and DCAR2.

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Source
http://dx.doi.org/10.1016/j.bbrc.2015.09.146DOI Listing

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