PMID- 19798032
OWN - NLM
STAT- MEDLINE
DCOM- 20091222
LR  - 20211020
IS  - 1759-4804 (Electronic)
IS  - 1759-4790 (Print)
IS  - 1759-4790 (Linking)
VI  - 5
IP  - 10
DP  - 2009 Oct
TI  - Dendritic cells as targets for therapy in rheumatoid arthritis.
PG  - 566-71
LID - 10.1038/nrrheum.2009.185 [doi]
AB  - Dendritic cells (DCs) are central in inducing immunity and in mediating immune 
      tolerance in their role as professional antigen-presenting cells. In the absence 
      of DCs, a fatal autoimmunity develops in animal models. Although the role of DCs 
      has been investigated extensively in the pathogenesis of rheumatoid arthritis 
      (RA), it remains unclear whether DCs initiate autoimmunity in this disease. 
      Nevertheless, evidence points towards a significant role for DCs in disease 
      maintenance and progression. Current biologic therapies target cytokine products 
      of antigen-presenting cells, such as tumor necrosis factor, interleukin-1 and 
      interleukin-6. Emerging therapies for RA exploit the tolerogenic capacity of DCs. 
      'Tolerogenic' DCs can be generated from myeloid precursors ex vivo, loaded with 
      antigen, and manipulated to suppress autoimmune responses in vivo, through the 
      induction of activation-induced cell death, anergy, and/or regulatory T cells. 
      Cells that are primed by DCs, such as B cells, type 1 and type 17 T helper cells, 
      and that have been implicated in certain models of autoimmunity, are also being 
      considered as additional targets for immune-based therapy. Studies to validate 
      these approaches to ameliorate autoimmunity will be necessary before their 
      application in the clinic.
FAU - Khan, Shaukat
AU  - Khan S
AD  - Cancer Institute, New York University Langone Medical Center, and New York 
      University Hospital for Joint Diseases, New York, NY 10016, USA.
FAU - Greenberg, Jeffrey D
AU  - Greenberg JD
FAU - Bhardwaj, Nina
AU  - Bhardwaj N
LA  - eng
GR  - R01 AI071078/AI/NIAID NIH HHS/United States
GR  - P01 AI057127-050002/AI/NIAID NIH HHS/United States
GR  - R01 AI061684-05/AI/NIAID NIH HHS/United States
GR  - R01 AI061684/AI/NIAID NIH HHS/United States
GR  - R01 AI071078-03/AI/NIAID NIH HHS/United States
GR  - P01 AI057127/AI/NIAID NIH HHS/United States
GR  - R37 AI044628-11/AI/NIAID NIH HHS/United States
GR  - R01 AIO71078/PHS HHS/United States
GR  - RC1 AI087097-02/AI/NIAID NIH HHS/United States
GR  - R37 AI044628/AI/NIAID NIH HHS/United States
GR  - RC1 AI087097/AI/NIAID NIH HHS/United States
PT  - Journal Article
PT  - Research Support, N.I.H., Extramural
PT  - Research Support, Non-U.S. Gov't
PT  - Review
PL  - United States
TA  - Nat Rev Rheumatol
JT  - Nature reviews. Rheumatology
JID - 101500080
RN  - 0 (Antirheumatic Agents)
SB  - IM
MH  - Animals
MH  - Antirheumatic Agents/*therapeutic use
MH  - Arthritis, Rheumatoid/*drug therapy/immunology
MH  - Autoimmunity/drug effects/immunology
MH  - Dendritic Cells/*drug effects/immunology/metabolism
MH  - Disease Models, Animal
MH  - *Drug Delivery Systems
MH  - *Drug Design
MH  - Humans
MH  - Immune Tolerance/*drug effects
PMC - PMC2884969
MID - NIHMS203323
COIS- Competing interests: None
EDAT- 2009/10/03 06:00
MHDA- 2009/12/23 06:00
PMCR- 2010/06/14
CRDT- 2009/10/03 06:00
PHST- 2009/10/03 06:00 [entrez]
PHST- 2009/10/03 06:00 [pubmed]
PHST- 2009/12/23 06:00 [medline]
PHST- 2010/06/14 00:00 [pmc-release]
AID - nrrheum.2009.185 [pii]
AID - 10.1038/nrrheum.2009.185 [doi]
PST - ppublish
SO  - Nat Rev Rheumatol. 2009 Oct;5(10):566-71. doi: 10.1038/nrrheum.2009.185.