PMID- 8423396
OWN - NLM
STAT- MEDLINE
DCOM- 19930219
LR  - 20190723
IS  - 0022-202X (Print)
IS  - 0022-202X (Linking)
VI  - 100
IP  - 1
DP  - 1993 Jan
TI  - Sunlight and skin-associated lymphoid tissues (SALT): if UVB is the trigger and 
      TNF alpha is its mediator, what is the message?
PG  - 47S-52S
AB  - The damaging effects on cutaneous immunity of low-dose ultraviolet B (UVB) 
      radiation in sunlight are genetically determined in mice. Polymorphic alleles at 
      the Tnf alpha and Lps loci dictate whether mice are UVB susceptible or resistant, 
      i.e., develop contact hypersensitivity or not when hapten is painted on 
      UVB-exposed skin. In mice, UVB susceptibility is mediated almost exclusively by 
      tumor necrosis factor-alpha (TNF alpha). Circumstantial evidence implicates 
      urocanic acid (UCA) in the stratum corneum as the photoreceptor for UVB, and 
      recent results suggest that cis-UCA in turn instigates the intraepidermal 
      accumulation of TNF alpha. It is hypothesized that TNF alpha interrupts the 
      induction of contact hypersensitivity by preventing epidermal Langerhans cells 
      from carrying hapten to the draining lymph node, where activation of naive, 
      hapten-specific T cells must first occur. The phenotypic traits of UVB 
      susceptibility (UVB-S) and UVB resistance (UVB-R) have now been documented in 
      human beings, and the frequency of UVB-S is high (approximately 40-45%) in both 
      Caucasians and individuals with deeply pigmented skin. Because the frequency of 
      UVB-S is extremely high in patients with biopsy-proved basal and squamous cell 
      skin cancer, this trait appears to be a risk factor for this disease. The 
      unexpectedly high frequency of UVB-S in human beings, including black-skinned 
      persons, implies that the trait is not perceived by evolutionary processes as 
      deleterious. The possible selective advantages conferred by alleles that 
      determine UVB-S are discussed with respect to cutaneous infections in which 
      mortality and morbidity are primarily mediated by immunopathogenic processes.
FAU - Streilein, J W
AU  - Streilein JW
AD  - Department of Microbiology and Immunology, University of Miami School of 
      Medicine, Florida 33101.
LA  - eng
GR  - AI22072/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.
PT  - Review
PL  - United States
TA  - J Invest Dermatol
JT  - The Journal of investigative dermatology
JID - 0426720
RN  - 0 (Tumor Necrosis Factor-alpha)
SB  - IM
MH  - Animals
MH  - Dermatitis, Contact/genetics/immunology
MH  - Disease Susceptibility
MH  - Humans
MH  - Immune System/radiation effects
MH  - Immunogenetics
MH  - Lymphoid Tissue/*radiation effects
MH  - Radiation Injuries, Experimental/genetics/immunology
MH  - Skin/*radiation effects
MH  - *Sunlight
MH  - Tumor Necrosis Factor-alpha/*physiology
MH  - *Ultraviolet Rays
RF  - 25
EDAT- 1993/01/01 00:00
MHDA- 1993/01/01 00:01
CRDT- 1993/01/01 00:00
PHST- 1993/01/01 00:00 [pubmed]
PHST- 1993/01/01 00:01 [medline]
PHST- 1993/01/01 00:00 [entrez]
AID - 10.1111/1523-1747.ep12355578 [doi]
PST - ppublish
SO  - J Invest Dermatol. 1993 Jan;100(1):47S-52S. doi: 10.1111/1523-1747.ep12355578.