PMID- 10692050
OWN - NLM
STAT- MEDLINE
DCOM- 20000315
LR  - 20190513
IS  - 0019-2805 (Print)
IS  - 1365-2567 (Electronic)
IS  - 0019-2805 (Linking)
VI  - 99
IP  - 2
DP  - 2000 Feb
TI  - Studies on delayed systemic effects of ultraviolet B radiation on the induction 
      of contact hypersensitivity, 3. Dendritic cells from secondary lymphoid organs 
      are deficient in interleukin-12 production and capacity to promote activation and 
      differentiation of T helper type 1 cells.
PG  - 296-304
AB  - Ultraviolet-B radiation (UVR) of mouse skin promotes both local and systemic 
      immune aberrations that are thought to be important in the pathogenesis of 
      cutaneous malignancies. Acute, low-dose UVR regimens inhibit the induction of 
      contact hypersensitivity (CH) in genetically susceptible mice by 
      TNF-alpha-dependent mechanisms. In addition, these regimens also promote the 
      development of tolerance when hapten is applied to the UVR-exposed site at the 
      completion of the radiation treatment protocol. A third immune abnormality is 
      also observed in mice exposed to acute, low-dose UVR. This abnormality, which 
      develops within 48-72 hr of the completion of the UVR regimen, has been described 
      among antigen-presenting cells within secondary lymphoid organs, including lymph 
      nodes that do not drain the site of irradiation. Dendritic cells (DCs) from lymph 
      nodes and spleens of mice exposed to UVR lack the capacity to induce CH if they 
      are derivatized with hapten and injected intracutaneously into naive mice. The DC 
      defect is related to the production of and systemic dissemination of 
      interleukin-10 (IL-10) by keratinocytes within the epidermis of the UVR-exposed 
      skin. We have now examined the nature of the functional aberration that exists 
      among DCs within the secondary lymphoid organs of UVR-exposed mice by examining 
      the capacity of DCs to express co-stimulatory molecules, and their ability to 
      activate ovalbumin (OVA) -specific DO11.10 T-cell receptor transgenic T cells in 
      vitro. Our results indicate that DCs from UVR-exposed mice produced insufficient 
      amounts of IL-12. When pulsed with OVA, these cells were capable of inducing 
      proliferation among DO11.10 T cells in vitro, but the responding cells produced 
      neither IFN-gamma nor IL-10 and IL-4. A similar antigen-presenting cell defect 
      was generated in mice treated with a subcutaneous injection of IL-10. We conclude 
      that acute, low-dose UVR creates an IL-10-dependent functional deficit in DCs in 
      secondary lymphoid organs, and that this defect robs UVR-exposed mice of the 
      capacity to develop CH when hapten is painted epicutaneously.
FAU - Kitazawa, T
AU  - Kitazawa T
AD  - The Schepens Eye Research Institute & Department of Dermatology, Harvard Medical 
      School, Boston, MA 02114, USA.
FAU - Streilein, J W
AU  - Streilein JW
LA  - eng
GR  - AR 44130/AR/NIAMS NIH HHS/United States
PT  - Journal Article
PT  - Research Support, U.S. Gov't, P.H.S.
PL  - England
TA  - Immunology
JT  - Immunology
JID - 0374672
RN  - 0 (CD40 Antigens)
RN  - 0 (Ligands)
RN  - 0 (Membrane Glycoproteins)
RN  - 130068-27-8 (Interleukin-10)
RN  - 147205-72-9 (CD40 Ligand)
RN  - 187348-17-0 (Interleukin-12)
RN  - 82115-62-6 (Interferon-gamma)
SB  - IM
MH  - Animals
MH  - Antigen Presentation
MH  - CD40 Antigens/metabolism
MH  - CD40 Ligand
MH  - Cell Culture Techniques
MH  - Dendritic Cells/*radiation effects
MH  - Dermatitis, Contact/*immunology
MH  - Interferon-gamma/pharmacology
MH  - Interleukin-10/immunology
MH  - Interleukin-12/*biosynthesis
MH  - Ligands
MH  - Lymphocyte Activation/drug effects
MH  - Membrane Glycoproteins/metabolism
MH  - Mice
MH  - Mice, Inbred BALB C
MH  - Th1 Cells/*immunology
MH  - *Ultraviolet Rays
PMC - PMC2327148
EDAT- 2000/02/26 09:00
MHDA- 2000/03/18 09:00
PMCR- 2001/02/01
CRDT- 2000/02/26 09:00
PHST- 2000/02/26 09:00 [pubmed]
PHST- 2000/03/18 09:00 [medline]
PHST- 2000/02/26 09:00 [entrez]
PHST- 2001/02/01 00:00 [pmc-release]
AID - imm951 [pii]
AID - 10.1046/j.1365-2567.2000.00951.x [doi]
PST - ppublish
SO  - Immunology. 2000 Feb;99(2):296-304. doi: 10.1046/j.1365-2567.2000.00951.x.