Characterization of FcεRI-bearing CD123+ blood dendritic cell antigen-2+ plasmacytoid dendritic cells in atopic dermatitis

2004 ◽  
Vol 114 (2) ◽  
pp. 364-370 ◽  
Author(s):  
Natalija Novak ◽  
Jean-Pierre Allam ◽  
Tobias Hagemann ◽  
Claudia Jenneck ◽  
Sylvia Laffer ◽  
...  
2014 ◽  
Vol 192 (12) ◽  
pp. 5789-5801 ◽  
Author(s):  
Craig P. Chappell ◽  
Natalia V. Giltiay ◽  
Kevin E. Draves ◽  
ChangHung Chen ◽  
Martha S. Hayden-Ledbetter ◽  
...  

Glycobiology ◽  
2018 ◽  
Vol 28 (8) ◽  
pp. 592-600 ◽  
Author(s):  
Jong-won Kim ◽  
James Budzak ◽  
Yu Liu ◽  
Sabine A F Jégouzo ◽  
Kurt Drickamer ◽  
...  

Abstract Blood dendritic cell antigen 2 (BDCA-2) is a C-type lectin found on the surface of plasmacytoid dendritic cells. It functions as a glycan-binding receptor that downregulates the production of type I interferons and thus plays a role in oligosaccharide-mediated immunomodulation. The carbohydrate recognition domain in BDCA-2 binds selectively to galactose-terminated bi-antennary glycans. Because the plasmacytoid dendritic cells function in a plasma environment rich in glycoproteins, experiments have been undertaken to identify endogenous ligands for blood dendritic cell antigen 2. A combination of blotting, affinity chromatography and proteomic analysis reveals that serum glycoprotein ligands for BDCA-2 include IgG, IgA and IgM. Compared to binding of IgG, which was previously described, IgA and IgM bind with higher affinity. The association constants for the different subclasses of immunoglobulins are below and roughly proportional to the serum concentrations of these glycoprotein ligands. Binding to the other main serum glycoprotein ligand, α2-macroglobulin, is independent of whether this protease inhibitor is activated. Binding to all of these glycoprotein ligands is mediated predominantly by bi-antennary glycans in which each branch bears a terminal galactose residue. The different affinities of the glycoprotein ligands reflect the different numbers of these galactose-terminated glycans and their degree of exposure on the native glycoproteins. The results suggest that normal serum levels of immunoglobulins could downmodulate interferon stimulation of further antibody production.


Hepatology ◽  
2013 ◽  
Vol 57 (5) ◽  
pp. 1705-1715 ◽  
Author(s):  
Sachiyo Yoshio ◽  
Tatsuya Kanto ◽  
Shoko Kuroda ◽  
Tokuhiro Matsubara ◽  
Koyo Higashitani ◽  
...  

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 ◽  
...  

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.


2009 ◽  
Vol 123 (1) ◽  
pp. 209-216.e4 ◽  
Author(s):  
Stephanie T. Yerkovich ◽  
Marjut Roponen ◽  
Miranda E. Smith ◽  
Kathy McKenna ◽  
Anthony Bosco ◽  
...  

2015 ◽  
Vol 27 (8) ◽  
pp. 2502-2510 ◽  
Author(s):  
Ünsal Yapici ◽  
Jesper Kers ◽  
Ivana Slavujevic-Letic ◽  
Geurt Stokman ◽  
Joris J.T.H. Roelofs ◽  
...  

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 ◽  
...  

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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