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Abstract: Myeloid dendritic cells, including BDCA3hi DCs and BDCA1+ DCs (hereafter dubbed DC1 and DC2 for clarity), play a pivotal role in the induction and regulation of immune responses. Interestingly, a fraction of DC2 also express low to intermediate levels of BDCA3. It is unknown whether BDCA3+ DC2 also share other traits with DC1 that are absent in BDCA3− DC2 and/or whether BDCA3 expression renders DC2 functionally distinct from their BDCA3‐lacking counterparts. Here, we used expression analysis on a predefined set of immunology‐related genes to determine divergence between BDCA3‐positive and BDCA3‐negative DC2 and their relation to bona fide BDCA3hi DC1. Results showed that mRNA fingerprints of BDCA3+ DC2 and BDCA3− DC2 are very similar, and clearly distinct from that of DC1. Differences in mRNA expression, however, were observed between BDCA3+ DC2 and BDCA3− DC2 that pointed toward a more activated status of BDCA3+ DC2. In line with this, higher steady state maturation marker expression and TLR‐induced maturation marker expression and inflammatory cytokine production by BDCA3+ DC2 were observed. This dataset provides insight into the relationship between myeloid DC populations and contributes to further understanding of DC immunobiology. [ABSTRACT FROM AUTHOR]

Myeloid dendritic cells, including BDCA3 hi DCs and BDCA1 + DCs (hereafter dubbed DC1 and DC2 for clarity), play a pivotal role in the induction and regulation of immune responses. Interestingly, a fraction of DC2 also express low to intermediate levels of BDCA3. It is unknown whether BDCA3 + DC2 also share other traits with DC1 that are absent in BDCA3 - DC2 and/or whether BDCA3 expression renders DC2 functionally distinct from their BDCA3-lacking counterparts. Here, we used expression analysis on a predefined set of immunology-related genes to determine divergence between BDCA3-positive and BDCA3-negative DC2 and their relation to bona fide BDCA3 hi DC1. Results showed that mRNA fingerprints of BDCA3 + DC2 and BDCA3 - DC2 are very similar, and clearly distinct from that of DC1. Differences in mRNA expression, however, were observed between BDCA3 + DC2 and BDCA3 - DC2 that pointed toward a more activated status of BDCA3 + DC2. In line with this, higher steady state maturation marker expression and TLR-induced maturation marker expression and inflammatory cytokine production by BDCA3 + DC2 were observed. This dataset provides insight into the relationship between myeloid DC populations and contributes to further understanding of DC immunobiology., (© 2017 The Authors Immunology & Cell Biology published by John Wiley & Sons Australia, Ltd on behalf of Australasian Society for Immunology Inc.)

Downregulation of major histocompatibility complex (MHC) molecules by tumor cells impairs cellular immune recognition and contributes to inefficient cell-mediated tumor eradication. Low or lack of expression of MHC molecules is frequently observed in early developmental or embryonically derived tumor cells. Considering the central role of the class II transactivator (CIITA) in MHC class II- and class I-mediated antigen presentation, we compared the induction of CIITA by interferon-gamma (IFN-gamma) in a diverse panel of developmental and more differentiated tumor cell lines. In contrast to the more differentiated tumor cell lines, none of the developmental tumor cell lines were capable of expressing CIITA after treatment with IFN-gamma. Remarkably, in transient transfection assays, CIITA promoter IV (CIITA-PIV) was found to be induced by IFN-gamma. Southern blot analysis of genomic DNA obtained from the developmental tumor cell lines indicated that the absence of endogenous CIITA induction was due to methylation of the CIITA-PIV region. Exposure to 5-azacytidine restored induction of CIITA and congruent HLA-DRA expression in these cells. The observation that only developmental tumor cell lines, originating from various tissues, employ methylation to silence CIITA expression may reflect the natural status of CIITA expression during early development rather than oncogenic transformation., (Copyright 2001 Wiley-Liss, Inc.)