INVESTIGADORES
CEBALLOS Ana
artículos
Título:
Epithelial Cells Activate Plasmacytoid Dendritic Cells Improving Their Anti-HIV Activity
Autor/es:
22. CHRISTIAN RODRIGUEZ RODRIGUES; MERCEDES CABRINI; FEDERICO REMES LENICOV; JUAN SABATTE; ANA CEBALLOS; ANTONELA MERLOTTI; JORGE GEFFNER
Revista:
PLOS ONE
Editorial:
PUBLIC LIBRARY SCIENCE
Referencias:
Lugar: San Francisco; Año: 2011 p. 6 - 8
ISSN:
1932-6203
Resumen:
Plasmacytoid dendritic cells (pDCs) play a major role in anti-viral immunity by virtue of their ability to produce high amounts
of type I interferons (IFNs) and a variety of inflammatory cytokines and chemokines in response to viral infections. Since
recent studies have established that pDCs accumulate at the site of virus entry in the mucosa, here we analyzed whether
epithelial cells were able to modulate the function of pDCs. We found that the epithelial cell lines HT-29 and Caco-2, as well
as a primary culture of human renal tubular epithelial cells (HRTEC), induced the phenotypic maturation of pDCs stimulating
the production of inflammatory cytokines. By contrast, epithelial cells did not induce any change in the phenotype of
conventional or myeloid DCs (cDCs) while significantly stimulated the production of the anti-inflammatory cytokine IL-10.
Activation of pDCs by epithelial cells was prevented by Bafilomycin A1, an inhibitor of endosomal acidification as well as by
the addition of RNase to the culture medium, suggesting the participation of endosomal TLRs. Interestingly, the cross-talk
between both cell populations was shown to be associated to an increased expression of TLR7 and TLR9 by pDCs and the
production of LL37 by epithelial cells, an antimicrobial peptide able to bind and transport extracellular nucleic acids into the
endosomal compartments. Interestingly, epithelium-activated pDCs impaired the establishment of a productive HIV
infection in two susceptible target cells through the stimulation of the production of type I IFNs, highlighting the anti-viral
efficiency of this novel activation pathway.