scholarly journals Reply to “Clusters of CD123+ plasmacytoid dendritic cells help distinguish lupus alopecia from lichen planopilaris”: Plasmacytoid dendritic cell content, clustering, and distribution pattern are useful parameters in differentiating lupus alopecia from lichen planopilaris

2017 ◽  
Vol 76 (2) ◽  
pp. e63
Author(s):  
Ossama Abbas
Keyword(s):  
Dendritic Cells ◽  
Dendritic Cell ◽  
Distribution Pattern ◽  
Plasmacytoid Dendritic Cell ◽  
Plasmacytoid Dendritic Cells ◽  
Cell Content ◽  
Lichen Planopilaris ◽  
Content Clustering

SPIB, a novel immunohistochemical marker for human blastic plasmacytoid dendritic cell neoplasms: characterization of its expression in major hematolymphoid neoplasms

Blood ◽  
2013 ◽  
Vol 121 (4) ◽  
pp. 643-647 ◽  
Author(s):  
Santiago Montes-Moreno ◽  
Rocio Ramos-Medina ◽  
Azahara Martínez-López ◽  
Carlos Barrionuevo Cornejo ◽  
Alejandro Parra Cubillos ◽  
...  
Keyword(s):  
Dendritic Cells ◽  
Transcription Factor ◽  
T Cell ◽  
Dendritic Cell ◽  
Cell Lymphoma ◽  
Plasmacytoid Dendritic Cell ◽  
Plasmacytoid Dendritic Cells ◽  
Ets Transcription Factor ◽  
Hematolymphoid Neoplasms

Abstract SPIB is an Ets transcription factor that is expressed exclusively in mature B cells, T-cell progenitors, and plasmacytoid dendritic cells. In the present study, we developed a novel mAb against the SPIB protein and characterized its expression in major hematolymphoid neoplasms, including a series of 45 cases of blastic plasmacytoid dendritic cell (BPDC) neoplasms and their potential cutaneous mimics. We found that SPIB is expressed heterogeneously among B- and T-cell lymphoma types. Interestingly, SPIB is expressed in a large proportion of nongerminal center type DLBCLs. In cutaneous neoplasms, SPIB is overexpressed in all BPDC neoplasms, but none of its cutaneous mimics. SPIB remains overexpressed in all cases that lack 1 or 2 of the markers used for BPDC neoplasms (ie, CD4, CD56, TCL1, and CD123). We conclude that SPIB expression can be used as a tool for diagnosing BPDC neoplasms, but it needs to be tested in conjunction with the growing arsenal of markers for human plasmacytoid dendritic cells.

scholarly journals BDCA-2, a Novel Plasmacytoid Dendritic Cell–specific Type II C-type Lectin, Mediates Antigen Capture and Is a Potent Inhibitor of Interferon α/β Induction

2001 ◽  
Vol 194 (12) ◽  
pp. 1823-1834 ◽  
Author(s):  
Andrzej Dzionek ◽  
Yoshiaki Sohma ◽  
Jun Nagafune ◽  
Marina Cella ◽  
Marco Colonna ◽  
...  
Keyword(s):  
Systemic Lupus Erythematosus ◽  
Dendritic Cells ◽  
Monoclonal Antibodies ◽  
Dendritic Cell ◽  
Lupus Erythematosus ◽  
Plasmacytoid Dendritic Cell ◽  
Plasmacytoid Dendritic Cells ◽  
Interferon Α ◽  
Type Ii ◽  
Systemic Lupus

Plasmacytoid dendritic cells are present in lymphoid and nonlymphoid tissue and contribute substantially to both innate and adaptive immunity. Recently, we have described several monoclonal antibodies that recognize a plasmacytoid dendritic cell-specific antigen, which we have termed BDCA-2. Molecular cloning of BDCA-2 revealed that BDCA-2 is a novel type II C-type lectin, which shows 50.7% sequence identity at the amino acid level to its putative murine ortholog, the murine dendritic cell–associated C-type lectin 2. Anti–BDCA-2 monoclonal antibodies are rapidly internalized and efficiently presented to T cells, indicating that BDCA-2 could play a role in ligand internalization and presentation. Furthermore, ligation of BDCA-2 potently suppresses induction of interferon α/β production in plasmacytoid dendritic cells, presumably by a mechanism dependent on calcium mobilization and protein-tyrosine phosphorylation by src-family protein-tyrosine kinases. Inasmuch as production of interferon α/β by plasmacytoid dendritic cells is considered to be a major pathophysiological factor in systemic lupus erythematosus, triggering of BDCA-2 should be evaluated as therapeutic strategy for blocking production of interferon α/β in systemic lupus erythematosus patients.

scholarly journals A type I IFN–Flt3 ligand axis augments plasmacytoid dendritic cell development from common lymphoid progenitors

2013 ◽  
Vol 210 (12) ◽  
pp. 2515-2522 ◽  
Author(s):  
Yi-Ling Chen ◽  
Ting-Ting Chen ◽  
Li-Mei Pai ◽  
Joanna Wesoly ◽  
Hans A.R. Bluyssen ◽  
...  
Keyword(s):  
Dendritic Cells ◽  
Dendritic Cell ◽  
Type I Interferon ◽  
Plasmacytoid Dendritic Cell ◽  
Critical Role ◽  
Plasmacytoid Dendritic Cells ◽  
Type I ◽  
Type I Ifn ◽  
Flt3 Ligand ◽  
Lymphoid Progenitors

During infections and inflammation, plasmacytoid dendritic cells (pDCs) are the most potent type I interferon (IFN-I)–producing cells. However, the developmental origin of pDCs and the signals dictating pDC generation remain incompletely understood. Here, we report a synergistic role for IFN-I and Flt3 ligand (FL) in pDC development from common lymphoid progenitors (CLPs). Both conventional DCs (cDCs) and pDCs were generated from CLPs in response to FL, whereas pDC generation required higher concentrations of FL and concurrent IFN-I signaling. An absence of IFN-I receptor, impairment of IFN-I signaling, or neutralization of IFN-I significantly impeded pDC development from CLPs. Furthermore, FL induced IFN-I expression in CLPs, which in turn induced Flt3 up-regulation that facilitated survival and proliferation of CLPs, as well as their differentiation into pDCs. Collectively, these results define a critical role for the FL/IFN-I/Flt3 axis in pDC differentiation from CLPs.

scholarly journals Plasmacytoid dendritic cells inhibit pulmonary immunopathology and promote clearance of respiratory syncytial virus

2006 ◽  
Vol 203 (5) ◽  
pp. 1153-1159 ◽  
Author(s):  
Joost J. Smit ◽  
Brian D. Rudd ◽  
Nicholas W. Lukacs
Keyword(s):  
Dendritic Cells ◽  
Respiratory Syncytial Virus ◽  
Dendritic Cell ◽  
Immune Responses ◽  
Plasmacytoid Dendritic Cell ◽  
Protective Role ◽  
Plasmacytoid Dendritic Cells ◽  
Rsv Infection ◽  
Syncytial Virus ◽  
Acquired Immune Responses

Respiratory syncytial virus (RSV) infection is widely spread and is a major cause of bronchiolitis in infants and high-risk adults, often leading to hospitalization. RSV infection leads to obstruction and inflammation of the airways and induction of innate and acquired immune responses. Because dendritic cells (DCs) are essential in the elicitation of these immune responses, we investigated the presence and the role of dendritic cell subtypes upon RSV infection in the lung. Here, we report that RSV infection increased the number of both conventional and plasmacytoid dendritic cells in the lung and the lung-draining lymph nodes. In particular, the increase in plasmacytoid dendritic cell numbers was sustained and lasted until 30 d after infection. Depletion of plasmacytoid dendritic cells resulted in decreased RSV clearance. In addition, depletion of plasmacytoid dendritic cells resulted in an exacerbation of all manifestations of immune-mediated pathology caused by RSV infection. In conclusion, this study demonstrates that both conventional and plasmacytoid dendritic cells are attracted to the site of RSV infection. It is demonstrated that plasmacytoid dendritic cells play a protective role during RSV infection by modulation of local immune responses.

scholarly journals Diagnostic utility of plasmacytoid dendritic cells in dermatopathology

2021 ◽  
Vol 87 ◽  
pp. 3-13
Author(s):  
Tara Bardawil ◽  
Samar Khalil ◽  
Mazen Kurban ◽  
Ossama Abbas
Keyword(s):  
Dendritic Cells ◽  
Dendritic Cell ◽  
Plasmacytoid Dendritic Cell ◽  
Protein A ◽  
Surrogate Marker ◽  
Plasmacytoid Dendritic Cells ◽  
Current Evidence ◽  
Histopathological Diagnosis ◽  
Type I ◽  
Resistance Protein

Differentiating cutaneous diseases that mimic each other clinically and histopathologically can at times be a challenging task for the dermatopathologist. At the same time, differentiation of entities with overlapping features may be crucial for patient management. Although not seen in normal skin, plasmacytoid dendritic cells usually infiltrate the skin in several infectious, inflammatory/autoimmune and neoplastic entities. Plasmacytoid dendritic cells can be identified in tissue using specific markers such as CD123 and/or blood-derived dendritic cell antigen-2. Plasmacytoid dendritic cells are the most potent producers of type I interferons and their activity may therefore be assessed indirectly in tissue using human myxovirus resistance protein A, a surrogate marker for type I interferon production. In recent years, accumulating evidence has established the utility of evaluating for specific plasmacytoid dendritic cell-related parameters (plasmacytoid dendritic cell content, distribution and clustering and/ or human myxovirus resistance protein A expression) as a diagnostic tool in differentiating cutaneous diseases with overlapping features such as the alopecias, lupus and its mimics, and neoplastic entities. In this review, we provide an update on the current evidence on this topic and on the contexts where this can be a useful adjunct to reach the histopathological diagnosis.

scholarly journals Type I Interferon Inhibition and Dendritic Cell Activation during Gammaherpesvirus Respiratory Infection

2007 ◽  
Vol 81 (18) ◽  
pp. 9778-9789 ◽  
Author(s):  
Janet L. Weslow-Schmidt ◽  
Nancy A. Jewell ◽  
Sara E. Mertz ◽  
J. Pedro Simas ◽  
Joan E. Durbin ◽  
...  
Keyword(s):  
Dendritic Cells ◽  
Dendritic Cell ◽  
Cell Activation ◽  
Type I Interferon ◽  
Plasmacytoid Dendritic Cells ◽  
The Body ◽  
Type I ◽  
Type I Ifn ◽  
Dendritic Cell Activation ◽  
Murine Gammaherpesvirus

ABSTRACT The respiratory tract is a major mucosal site for microorganism entry into the body, and type I interferon (IFN) and dendritic cells constitute a first line of defense against viral infections. We have analyzed the interaction between a model DNA virus, plasmacytoid dendritic cells, and type I IFN during lung infection of mice. Our data show that murine gammaherpesvirus 68 (γHV68) inhibits type I IFN secretion by dendritic cells and that plasmacytoid dendritic cells are necessary for conventional dendritic cell maturation in response to γHV68. Following γHV68 intranasal inoculation, the local and systemic IFN-α/β response is below detectable levels, and plasmacytoid dendritic cells are activated and recruited into the lung with a tissue distribution that differs from that of conventional dendritic cells. Our results suggest that plasmacytoid dendritic cells and type I IFN have important but independent roles during the early response to a respiratory γHV68 infection. γHV68 infection inhibits type I IFN production by dendritic cells and is a poor inducer of IFN-α/β in vivo, which may serve as an immune evasion strategy.

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