Plasmacytoid Dendritic Cells Activate Lymphoid-Specific Genetic Programs Irrespective of Their Cellular Origin

Shigematsu, Hirokazu; Reizis, Boris; Iwasaki, Hiromi; Mizuno, Shin Ichi; Hu, Dan; Traver, David; Leder, Philip; Sakaguchi, Nobuo; Akashi, Koichi

doi:10.1016/j.immuni.2004.06.011

Cited by 212 publications

(214 citation statements)

References 60 publications

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“…Promiscuity in lineage commitment is not a new concept in B and myeloid TF literature (59). The hypothesis that PRDM1 is expressed in a common memory and plasma cell precursor has been published in the past (60).…”

Section: Irf4mentioning

confidence: 99%

Stages of Germinal Center Transit Are Defined by B Cell Transcription Factor Coexpression and Relative Abundance

Cattoretti

Shaknovich

Smith

et al. 2006

The Journal of Immunology

125

117

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The transit of T cell-activated B cells through the germinal center (GC) is controlled by sequential activation and repression of key transcription factors, executing the pre- and post-GC B cell program. B cell lymphoma (BCL) 6 and IFN regulatory factor (IRF) 8 are necessary for GC formation and for its molecular activity in Pax5+PU.1+ B cells. IRF4, which is highly expressed in BCL6− GC B cells, is necessary for class switch recombination and the plasma cell differentiation at exit from the GC. In this study, we show at the single-cell level broad coexpression of IRF4 with BCL6, Pax5, IRF8, and PU.1 in pre- and post-GC B cells in human and mouse. IRF4 is down-regulated in BCL6+ human GC founder cells (IgD+CD38+), is absent in GC centroblasts, and is re-expressed in positive regulatory domain 1-positive centrocytes, which are negative for all the B cell transcription factors. Activated (CD30+) and activation-induced cytidine deaminase-positive extrafollicular blasts coexpress Pax5 and IRF4. PU.1-negative plasma cells and CD30+ blasts uniquely display the conformational epitope of IRF4 recognized by the MUM1 Ab, an epitope that is absent from any other IRF4+PU.1+ lymphoid and hemopoietic subsets. Low grade B cell lymphomas, representing the malignant counterpart of pre- and post-GC B cells, accordingly express IRF4. However, a fraction of BCL6+ diffuse large B cell lymphomas express IRF4 bearing the MUM1 epitope, indicative of a posttranscriptional modification of IRF4 not seen in the normal counterpart.

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Section: Irf4mentioning

confidence: 99%

Stages of Germinal Center Transit Are Defined by B Cell Transcription Factor Coexpression and Relative Abundance

Cattoretti

Shaknovich

Smith

et al. 2006

The Journal of Immunology

125

117

View full text Add to dashboard Cite

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“…DCs were isolated according to a previously described protocol (18). Briefly, spleens were digested with 1 mg/ml collagenase D (Roche Diagnostics) and 50 g/ml DNase I (Sigma-Aldrich).…”

Section: Nk-dc Coculturementioning

confidence: 99%

NK Cells Enhance Dendritic Cell Response against Parasite Antigens via NKG2D Pathway

Guan

Moretto

Bzik

et al. 2007

The Journal of Immunology

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Recent studies have shown that NK-dendritic cell (DC) interaction plays an important role in the induction of immune response against tumors and certain viruses. Although the effect of this interaction is bidirectional, the mechanism or molecules involved in this cross-talk have not been identified. In this study, we report that coculture with NK cells causes several fold increase in IL-12 production by Toxoplasma gondii lysate Ag-pulsed DC. This interaction also leads to stronger priming of Ag-specific CD8+ T cell response by these cells. In vitro blockade of NKG2D, a molecule present on human and murine NK cells, neutralizes the NK cell-induced up-regulation of DC response. Moreover, treatment of infected animals with Ab to NKG2D receptor compromises the development of Ag-specific CD8+ T cell immunity and reduces their ability to clear parasites. These studies emphasize the critical role played by NKG2D in the NK-DC interaction, which apparently is important for the generation of robust CD8+ T cell immunity against intracellular pathogens. To the best of our knowledge, this is the first work that describes in vivo importance of NKG2D during natural infection.

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“…In accordance with their discrete roles in shaping an immune response [18], cDC and pDC express complementary yet distinct sets of TLR, resulting in a differential response to pathogens. Both cDC and pDC can be generated from either lymphoid or myeloid progenitors, but this potential is lost once definitive megakaryocyte-erythrocyte progenitor or B cell commitment occurs [19][20][21][22]. Thus, the DC lineage is much more developmentally flexible than other bone marrowderived leukocytes.…”

Section: Introductionmentioning

confidence: 99%

Type I interferon regulates pDC maturation and Ly49Q expression

Toma-Hirano

Namiki²,

Miyatake

et al. 2007

Eur J Immunol

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Ly49Q is expressed on peripheral mouse plasmacytoid dendritic cells (pDC). Immature Ly49Q-negative pDC precursors acquire Ly49Q in the bone marrow and then migrate into the periphery. While searching for molecules that regulate pDC maturation, we found that type I interferon (IFN) inhibited Ly49Q acquisition in vitro. Infections that induce type I IFN production by cells other than pDC (a condition mimicked by poly(I:C) injection in vivo) increase the prevalence of Ly49Q -pDC in the bone marrow and peripheral lymphoid organs in wild-type but not IFN-a/b receptor knockout BALB/c mice. Moreover, in vivo exposure to type I IFN causes some Ly49Q -, but not Ly49Q + , pDC to convert to conventional DC, defined as B220 -CD11c + CD11b + cells. These data suggest that type I IFN regulates pDC development and affects their distribution in the body.

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Plasmacytoid Dendritic Cells Activate Lymphoid-Specific Genetic Programs Irrespective of Their Cellular Origin

Cited by 212 publications

References 60 publications

Stages of Germinal Center Transit Are Defined by B Cell Transcription Factor Coexpression and Relative Abundance

Stages of Germinal Center Transit Are Defined by B Cell Transcription Factor Coexpression and Relative Abundance

NK Cells Enhance Dendritic Cell Response against Parasite Antigens via NKG2D Pathway

Type I interferon regulates pDC maturation and Ly49Q expression

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