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The mouse dendritic cell marker CD11c is down-regulated upon cell activation through Toll-like receptor triggering
- Source :
-
Immunobiology . Jan2013, Vol. 218 Issue 1, p28-39. 12p. - Publication Year :
- 2013
-
Abstract
- Abstract: Dendritic cells (DC) play a key role in regulating immune responses and are the best professional antigen-presenting cells. Two major DC populations are defined in part according to cell surface CD11c expression levels. Unexpectedly, we observed that mouse DC strongly down-regulate the typical DC marker CD11c upon activation. To better characterize DC responses, we have analyzed CD11c expression on mouse and human myeloid DC after Toll-like receptor (TLR) triggering. Here we show that mouse bone marrow-derived DC (BMDC) as well as spleen DC down-regulate cell surface CD11c upon activation by TLR3/4/9 agonists. In all cases, full DC activation was reached, as determined by cytokine secretion, cell stimulation in mixed leukocyte reactions (MLR), and CD40/CD86/major histocompatibility complex (MHC) up-regulation. Interestingly, membrane CD11c down-regulation correlated with increased cytoplasmic pools of CD11c. In contrast to the up-regulation of CD40 and MHC class II molecules, lipopolysaccharide (LPS)-induced CD11c down-regulation was MyD88-dependent. Polyinosinic–polycytidylic acid (poly I:C), which does not signal through MyD88, also induced cell surface CD11c down-regulation. Notably, CD11c down-regulation was not observed upon activation of human DC, either through TLR-dependent or -independent cell activation. Thus, activated mouse DC may be transiently CD11c-negative in vivo, hampering the identification of those cells. On the other hand, cell surface CD11c down-regulation may serve as a new activation marker for mouse DC. [Copyright &y& Elsevier]
Details
- Language :
- English
- ISSN :
- 01712985
- Volume :
- 218
- Issue :
- 1
- Database :
- Academic Search Index
- Journal :
- Immunobiology
- Publication Type :
- Academic Journal
- Accession number :
- 83868529
- Full Text :
- https://doi.org/10.1016/j.imbio.2012.01.021