PMID- 11496241
OWN - NLM
STAT- MEDLINE
DCOM- 20010906
LR  - 20131121
IS  - 0091-6749 (Print)
IS  - 0091-6749 (Linking)
VI  - 108
IP  - 2
DP  - 2001 Aug
TI  - Inhibition of human allergic T-cell responses by IL-10-treated dendritic cells: 
      differences from hydrocortisone-treated dendritic cells.
PG  - 242-9
AB  - BACKGROUND: Dendritic cells (DCs) are able to induce human allergic T(H)1 
      responses as well as T(H)2 responses. OBJECTIVE: In this study, we examined the 
      effect of antiinflammatory agents such as IL-10 and hydrocortisone (HC) on the 
      accessory function of DCs and the resulting T-cell response, especially that of 
      T(H)2 cells. METHODS: Naive and memory CD4(+) T cells from atopic donors were 
      stimulated with autologous allergen-pulsed DCs generated from CD14(+) monocytes 
      by culture with GM-CSF/IL-4 and fully matured with IL-1 beta, TNF-alpha, and 
      PGE(2) in the presence or absence of IL-10 or HC. RESULTS: IL-10-treated DCs and, 
      to a lesser extent, HC-treated DCs showed a decreased expression of MHC II 
      molecules, the costimulatory molecule CD86, and the DC-specific marker CD83, as 
      well as a strongly reduced IL-12 secretion. Consequently, T-cell proliferation 
      was reduced after stimulation with IL-10- or HC-treated DCs alike. However, 
      pretreatment of DCs with IL-10 inhibited the production of T(H)1 and T(H)2 
      cytokines by T cells, whereas HC-treated DCs inhibited production of IFN-gamma 
      but induced an increased release of IL-4 and no change in IL-5. Both effects were 
      long-lasting; cytokine production remained low (which was due not to enhanced 
      apoptosis but to functional hyporesponsiveness) or even increased after 
      restimulation with fully matured DCs. CONCLUSION: These data indicate that IL-10- 
      or HC-treated DCs differ in their ability to influence human allergic T-cell 
      responses. This has major implications for therapeutic strategies aiming at the 
      downregulation of proallergic T(H)2 responses.
FAU - Bellinghausen, I
AU  - Bellinghausen I
AD  - Department of Dermatology, University of Mainz, Germany.
FAU - Brand, U
AU  - Brand U
FAU - Steinbrink, K
AU  - Steinbrink K
FAU - Enk, A H
AU  - Enk AH
FAU - Knop, J
AU  - Knop J
FAU - Saloga, J
AU  - Saloga J
LA  - eng
PT  - Comparative Study
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - United States
TA  - J Allergy Clin Immunol
JT  - The Journal of allergy and clinical immunology
JID - 1275002
RN  - 0 (Allergens)
RN  - 0 (Anti-Inflammatory Agents)
RN  - 0 (Cytokines)
RN  - 0 (Interleukin-5)
RN  - 130068-27-8 (Interleukin-10)
RN  - 207137-56-2 (Interleukin-4)
RN  - 82115-62-6 (Interferon-gamma)
RN  - WI4X0X7BPJ (Hydrocortisone)
SB  - IM
MH  - Allergens
MH  - Anti-Inflammatory Agents/*pharmacology
MH  - Antigen Presentation
MH  - CD4-Positive T-Lymphocytes
MH  - Cytokines/biosynthesis
MH  - Dendritic Cells/*drug effects
MH  - Humans
MH  - Hydrocortisone/*pharmacology
MH  - Hypersensitivity, Immediate/*immunology
MH  - Immunologic Memory
MH  - Interferon-gamma/biosynthesis
MH  - Interleukin-10/*pharmacology
MH  - Interleukin-4/biosynthesis
MH  - Interleukin-5/biosynthesis
MH  - Models, Immunological
MH  - T-Lymphocytes/*immunology
MH  - Th2 Cells/drug effects
EDAT- 2001/08/10 10:00
MHDA- 2001/09/08 10:01
CRDT- 2001/08/10 10:00
PHST- 2001/08/10 10:00 [pubmed]
PHST- 2001/09/08 10:01 [medline]
PHST- 2001/08/10 10:00 [entrez]
AID - S0091-6749(01)83803-3 [pii]
AID - 10.1067/mai.2001.117177 [doi]
PST - ppublish
SO  - J Allergy Clin Immunol. 2001 Aug;108(2):242-9. doi: 10.1067/mai.2001.117177.