PMID- 21410666
OWN - NLM
STAT- MEDLINE
DCOM- 20111017
LR  - 20201226
IS  - 1365-2133 (Electronic)
IS  - 0007-0963 (Linking)
VI  - 165
IP  - 2
DP  - 2011 Aug
TI  - Interferon-alpha in the generation of monocyte-derived dendritic cells: recent 
      advances and implications for dermatology.
PG  - 247-54
LID - 10.1111/j.1365-2133.2011.10301.x [doi]
AB  - Dendritic cells (DCs) have a critical role in antiviral responses, in autoimmune 
      disease pathogenesis and in initiating and maintaining inflammatory skin 
      disorders, and are candidates for cell-based immunotherapeutic approaches for 
      tumours. Recent studies have shown the important role of type I interferons 
      (IFNs) in DC differentiation and activation. In the presence of IFN-alpha and 
      granulocyte/macrophage colony-stimulating factor monocytes differentiate into DCs 
      referred to as IFN-DCs. In vitro generated IFN-DCs show a partially mature 
      phenotype, are effective in taking up antigens, share features of myeloid DCs, 
      plasmacytoid DCs and natural killer cells, exhibit an enhanced chemotactic 
      response and are capable of migrating to the lymph nodes. IFN-DCs produce several 
      chemokines and cytokines, including T-helper 1 (Th1) mediators belonging to the 
      interleukin-12 family. IFN-DCs stimulate T- and B-cell responses and the 
      production of IFN-gamma in mixed lymphocyte reactions and have a capacity to produce 
      IFN-gamma themselves. IFN-DCs express several toll-like receptor (TLR) subtypes and 
      TLR ligand stimulation improves their costimulatory molecule expression, 
      increases their Th1 cytokine production and enhances their capacity to stimulate 
      naive T-cell proliferation. Here we review the interaction of IFN-alpha and monocytes 
      and the role of IFN-DCs in infections, in autoimmunity, in inflammation and in 
      cancer immunotherapy focusing on dermatological conditions.
CI  - (c) 2011 The Authors. BJD (c) 2011 British Association of Dermatologists 2011.
FAU - Farkas, A
AU  - Farkas A
AD  - Department of Dermatology and Allergology, University of Szeged, 6720 Szeged, 
      Hungary. farkas@mail.derma.szote.u-szeged.hu
FAU - Kemeny, L
AU  - Kemeny L
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PT  - Review
DEP - 20110602
PL  - England
TA  - Br J Dermatol
JT  - The British journal of dermatology
JID - 0004041
RN  - 0 (Interferon-alpha)
RN  - 0 (Toll-Like Receptors)
RN  - 81627-83-0 (Macrophage Colony-Stimulating Factor)
RN  - 83869-56-1 (Granulocyte-Macrophage Colony-Stimulating Factor)
SB  - IM
MH  - Cell Differentiation
MH  - Dendritic Cells/*cytology
MH  - Granulocyte-Macrophage Colony-Stimulating Factor/*physiology
MH  - Humans
MH  - Immunotherapy/methods
MH  - Interferon-alpha/biosynthesis/pharmacology/*physiology
MH  - Lupus Erythematosus, Systemic/etiology/pathology
MH  - Macrophage Colony-Stimulating Factor/*physiology
MH  - Monocytes/*cytology
MH  - Psoriasis/etiology/pathology
MH  - Skin Diseases/*pathology/*therapy
MH  - Skin Diseases, Viral/pathology
MH  - Skin Neoplasms/therapy
MH  - Toll-Like Receptors/metabolism
EDAT- 2011/03/18 06:00
MHDA- 2011/10/18 06:00
CRDT- 2011/03/18 06:00
PHST- 2011/03/18 06:00 [entrez]
PHST- 2011/03/18 06:00 [pubmed]
PHST- 2011/10/18 06:00 [medline]
AID - 10.1111/j.1365-2133.2011.10301.x [doi]
PST - ppublish
SO  - Br J Dermatol. 2011 Aug;165(2):247-54. doi: 10.1111/j.1365-2133.2011.10301.x. 
      Epub 2011 Jun 2.