PMID- 2098069
OWN - NLM
STAT- MEDLINE
DCOM- 19910731
LR  - 20131121
IS  - 0896-0623 (Print)
IS  - 0896-0623 (Linking)
VI  - 3
IP  - 3
DP  - 1990-1991
TI  - Tumor necrosis factor-alpha and ultraviolet B light have similar effects on 
      contact hypersensitivity in mice.
PG  - 139-44
AB  - Acute, low dose ultraviolet B (UVB) radiation impairs the induction of 
      dinitrofluorobenzene (DNFB)-specific contact hypersensitivity (CH) in some, but 
      not all, inbred strains of mice. Although C3H/HeN mice are UVB-susceptible by 
      these criteria, the closely related strain, C3H/HeJ proved to be UVB-resistant. 
      Since the only known important genetic difference between these strains is a 
      polymorphism at the Lps locus which governs sensitivity to bacterial 
      lipopolysaccharide (LPS), we examined the possibility that UVB radiation achieves 
      its immune effects via an action directly or indirectly related to LPS. We found 
      that intradermal injections of LPS failed to impair the induction of CH when DNFB 
      was painted at the skin injection site. However, tumor necrosis factor-alpha (TNF 
      alpha), a cytokine released from LPS-sensitive macrophages by exposure to LPS, 
      was able to suppress CH induction when it was injected intradermally (50 ng) 
      prior to epicutaneous application of hapten. In addition, systemic administration 
      of larger doses of TNF alpha (200 ng) inhibited CH, whether the cytokine was 
      injected intraperitoneally at the time of cutaneous sensitization with DNFB, or 
      prior to ear challenge with the hapten. Importantly, when TNF alpha was injected 
      into pinnae of DNFB-immune mice prior to elicitation of CH, local inflammatory 
      responses were greatly exaggerated. Thus, TNF alpha shares with acute, low dose 
      UVB radiation the following effects on CH: impairment of induction, and 
      amplification of expression. These effects are only achieved following local 
      treatment with these agents. We propose that TNF alpha is an important cytokine 
      mediator of the effects of UVB on hapten-specific CH.
FAU - Yoshikawa, T
AU  - Yoshikawa T
AD  - Department of Microbiology and Immunology, University of Miami School of 
      Medicine, FL 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, U.S. Gov't, P.H.S.
PL  - United States
TA  - Reg Immunol
JT  - Regional immunology
JID - 9001013
RN  - 0 (Lipopolysaccharides)
RN  - 0 (Recombinant Proteins)
RN  - 0 (Tumor Necrosis Factor-alpha)
RN  - D241E059U6 (Dinitrofluorobenzene)
SB  - IM
MH  - Animals
MH  - Dermatitis, Contact/*etiology/immunology/prevention & control
MH  - Dinitrofluorobenzene
MH  - Female
MH  - Lipopolysaccharides
MH  - Mice
MH  - Mice, Inbred BALB C
MH  - Mice, Inbred C3H
MH  - Recombinant Proteins/pharmacology
MH  - Skin/drug effects
MH  - Tumor Necrosis Factor-alpha/*pharmacology
MH  - *Ultraviolet Rays
EDAT- 1990/01/01 00:00
MHDA- 1990/01/01 00:01
CRDT- 1990/01/01 00:00
PHST- 1990/01/01 00:00 [pubmed]
PHST- 1990/01/01 00:01 [medline]
PHST- 1990/01/01 00:00 [entrez]
PST - ppublish
SO  - Reg Immunol. 1990-1991;3(3):139-44.