PMID- 1431236
OWN - NLM
STAT- MEDLINE
DCOM- 19921207
LR  - 20190723
IS  - 0022-202X (Print)
IS  - 0022-202X (Linking)
VI  - 99
IP  - 5
DP  - 1992 Nov
TI  - Deleterious effects of cis-urocanic acid and UVB radiation on Langerhans cells 
      and on induction of contact hypersensitivity are mediated by tumor necrosis 
      factor-alpha.
PG  - 69S-70S
AB  - Ultraviolet B (UVB) light disrupts epidermal Langerhans cells (LC) universally 
      and impairs the induction of contact hypersensitivity (CH) to epicutaneously 
      applied haptens in certain strains of mice. Similar effects are observed when 
      tumor necrosis factor-alpha (TNF alpha) is injected intradermally (ID) in mice. 
      Trans-urocanic acid (UCA), a photoreceptor for UVB radiation, is known to be 
      immunosuppressive. To determine whether cis-UCA is important in the process by 
      which UVB and/or TNF alpha act in the skin, cis-UCA was injected ID into C57BL/6, 
      C3H/HeN, BALB/c, and C3H/HeJ mice. Whole mounts of epidermis were removed 5 h 
      later and stained immunochemically with anti-Ia antibodies. Microscopy revealed 
      that Ia-bearing LC had lost their dendrites, had rounded up, and were reduced in 
      number in all strains examined. Moreover, when dinitrofluorobenzene (DNFB) was 
      applied epicutaneously to the injected site, induction of CH was grossly 
      impaired. When neutralizing anti-TNF alpha antibodies were administered 
      intraperitoneally 2 h prior to ID injection of cis-UCA, the deleterious effects 
      on LC and CH induction were largely reversed. These results indicate that the 
      actions of cis-UCA on LC and on CH induction are very similar to those achieved 
      by ID injections of TNF alpha and by cutaneous exposure to low-dose UVB. Because 
      the effects of UVB radiation and cis-UCA are reversed by anti-TNF alpha 
      antibodies, we propose that UVB radiation impairs the induction of CH in mice by 
      converting trans-UCA to cis-UCA within the epidermis; cis-UCA in turn causes the 
      local release of TNF alpha, which thwarts sensitization by its ability to alter 
      the functional program of epidermal Langerhans cells, thereby preventing the 
      induction of CH.
FAU - Kurimoto, I
AU  - Kurimoto I
AD  - Department of Microbiology and Immunology, University of Miami School of 
      Medicine, Florida 33101.
FAU - Streilein, J W
AU  - Streilein JW
LA  - eng
GR  - AI-22072/AI/NIAID NIH HHS/United States
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PT  - Research Support, U.S. Gov't, P.H.S.
PL  - United States
TA  - J Invest Dermatol
JT  - The Journal of investigative dermatology
JID - 0426720
RN  - 0 (Tumor Necrosis Factor-alpha)
RN  - D241E059U6 (Dinitrofluorobenzene)
RN  - G8D26XJJ3B (Urocanic Acid)
SB  - IM
MH  - Administration, Topical
MH  - Animals
MH  - Dermatitis, Contact/*etiology
MH  - Dinitrofluorobenzene/administration & dosage
MH  - Injections, Intradermal
MH  - Langerhans Cells/*drug effects/*radiation effects
MH  - Mice
MH  - Mice, Inbred BALB C
MH  - Mice, Inbred C3H
MH  - Mice, Inbred C57BL
MH  - Stereoisomerism
MH  - Time Factors
MH  - Tumor Necrosis Factor-alpha/*pharmacology
MH  - *Ultraviolet Rays
MH  - Urocanic Acid/*pharmacology
EDAT- 1992/11/01 00:00
MHDA- 1992/11/01 00:01
CRDT- 1992/11/01 00:00
PHST- 1992/11/01 00:00 [pubmed]
PHST- 1992/11/01 00:01 [medline]
PHST- 1992/11/01 00:00 [entrez]
AID - 0022-202X(92)90728-M [pii]
AID - 10.1111/1523-1747.ep12669754 [doi]
PST - ppublish
SO  - J Invest Dermatol. 1992 Nov;99(5):69S-70S. doi: 10.1111/1523-1747.ep12669754.