PMID- 8618036
OWN - NLM
STAT- MEDLINE
DCOM- 19960613
LR  - 20190723
IS  - 0022-202X (Print)
IS  - 0022-202X (Linking)
VI  - 106
IP  - 5
DP  - 1996 May
TI  - In vivo retinoic acid modulates expression of the class II major 
      histocompatibility complex and function of antigen-presenting macrophages and 
      keratinocytes in ultraviolet-exposed human skin.
PG  - 1042-6
AB  - Because retinoic acid (RA) can alter photoaging of the skin and repeated 
      ultraviolet (UV)-induced immunologic injury may play a role in chronic 
      photoaging, we asked whether RA alters the acute photoimmunologic effects of UV 
      radiation. Two sites from each volunteer were treated with 0.1% RA or vehicle 
      continuously for 24 h before and 24 h after a 4-minimal erythema dose UVB 
      exposure. RA did not function as a sunscreen, as determined by quantitating the 
      increase in redness after 1 minimal erythema dose to vehicle- and RA-pretreated 
      sites (n = 12). By flow cytometric analysis of epidermal cell suspensions 
      harvested 3 d after the UV-EC, RA treatment did not protect CD1+ Langerhans cells 
      from being depleted by UV light and did not modify the number of UV-induced 
      infiltrating CD36+CD11b+CD1-DR+ macrophages. RA treatment did, however, result in 
      a 40% downregulation of human leukocyte antigen (HLA)-DR expression on these 
      infiltrating macrophages (p = 0.016) (n = 11), in conjunction with a decrease in 
      alloantigen-presenting cell activity of RA-treated UV-EC as measured by T-cell 
      proliferations. RA also induced a 72% inhibition of the autologous T 
      suppressor-inducer cell proliferation induced by UV-EC (vehicle: 21,813 +/- 7,302 
      cpm; RA; 5,299 +/-635 cpm) (n = 3). The downregulation could be due to 
      RA-modulated keratinocytes; RA-treated UV-EC keratinocytes depleted of CD1a+ and 
      DR+ antigen-presenting cells displayed a greater ability, relative to similarly 
      treated vehicle-EC keratinocytes, to inhibit alloantigen presentation. IN 
      CONCLUSION: (i) in vivo RA treatment did not protect human Langerhans cells from 
      being depleted by UV and did not block infiltration of macrophages into sunburned 
      skin; and (ii) RA did decrease autologous and allogeneic T-cell reactivity 
      induced by macrophage antigen-presenting cells in UV-exposed epidermis, at least 
      in part by downregulating their HLA-DR expression and by upregulating inhibitory 
      signals from UV-irradiated keratinocytes.
FAU - Meunier, L
AU  - Meunier L
AD  - Department of Dermatology, University of Michigan, Ann Arbor, USA.
FAU - Voorhees, J J
AU  - Voorhees JJ
FAU - Cooper, K D
AU  - Cooper KD
LA  - eng
GR  - R01-AR41642/AR/NIAMS 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 (HLA-DR Antigens)
RN  - 5688UTC01R (Tretinoin)
SB  - IM
MH  - Adult
MH  - Female
MH  - HLA-DR Antigens/*analysis
MH  - Humans
MH  - Keratinocytes/drug effects/physiology/*radiation effects
MH  - Lymphocyte Activation/drug effects
MH  - Macrophages/drug effects/physiology/*radiation effects
MH  - Male
MH  - Middle Aged
MH  - Skin/*radiation effects
MH  - T-Lymphocytes/drug effects
MH  - Tretinoin/*pharmacology
MH  - *Ultraviolet Rays
EDAT- 1996/05/01 00:00
MHDA- 1996/05/01 00:01
CRDT- 1996/05/01 00:00
PHST- 1996/05/01 00:00 [pubmed]
PHST- 1996/05/01 00:01 [medline]
PHST- 1996/05/01 00:00 [entrez]
AID - S0022-202X(15)42554-0 [pii]
AID - 10.1111/1523-1747.ep12338626 [doi]
PST - ppublish
SO  - J Invest Dermatol. 1996 May;106(5):1042-6. doi: 10.1111/1523-1747.ep12338626.