PMID- 1607677
OWN - NLM
STAT- MEDLINE
DCOM- 19920722
LR  - 20190723
IS  - 0022-202X (Print)
IS  - 0022-202X (Linking)
VI  - 99
IP  - 1
DP  - 1992 Jul
TI  - Characterization of a glucocorticosteroid-induced inhibitor of interferon-gamma 
      induction of HLA-DR expression.
PG  - 35-9
AB  - Interferon gamma (IFN-gamma) induces human leukocyte antigen (HLA)-DR antigen 
      expression on a variety of cell types, and in human skin cells this induction is 
      inhibited by trypsin inhibitors. Recently a trypsin-like protease was 
      characterized whose activity is required for HLA-DR induction in a hybrid 
      epidermal cell line. Glucocorticosteroids also inhibit IFN-gamma-induced HLA-DR 
      expression, and similarities have been noted between the inhibition by trypsin 
      inhibitors and by glucocorticosteroids. To assess the possibility that 
      glucocorticosteroid inhibition of IFN-gamma-induced HLA-DR expression might be 
      due to induction of an inhibitor of trypsin activity that is re-expression, we 
      examined culture medium supernates (CM) of glucocorticosteroid-treated cells for 
      HLA-DR- and trypsin-inhibitory activities. We report here that CM of 
      glucocorticosteroid-treated H12 cells contain inhibitors of HLA-DR expression and 
      of trypsin activity, but that the two inhibitors are not identical. H12 cells 
      constitutively secrete a greater than 30,000 MW, acid- and heat-stable trypsin 
      inhibitor, whose expression is not modulated by glucocorticosteroid or IFN-gamma, 
      and that does not inhibit IFN-gamma-induced HLA-DR expression. The HLA-DR 
      inhibitor, on the other hand, is present only in CM of 
      glucocorticosteroid-treated cells, is distinct from glucocorticosteroid itself, 
      of a MW less than 500 and does not inhibit trypsin. We conclude, therefore, that 
      the glucocorticosteroid inhibition of IFN-gamma-induced HLA-DR expression is by a 
      mechanism other than secretion of a trypsin inhibitor.
FAU - Smith, B
AU  - Smith B
AD  - Department of Dermatology, University of California, Davis School of Medicine.
FAU - Berman, B
AU  - Berman B
LA  - eng
PT  - Journal Article
PT  - Research Support, U.S. Gov't, Non-P.H.S.
PL  - United States
TA  - J Invest Dermatol
JT  - The Journal of investigative dermatology
JID - 0426720
RN  - 0 (Glucocorticoids)
RN  - 0 (HLA-DR Antigens)
RN  - 0 (Interferon Inducers)
RN  - 0 (Trypsin Inhibitors)
RN  - 82115-62-6 (Interferon-gamma)
RN  - EC 3.4.21.73 (Urokinase-Type Plasminogen Activator)
SB  - IM
MH  - Cells, Cultured
MH  - Gene Expression Regulation
MH  - Glucocorticoids/*pharmacology
MH  - HLA-DR Antigens/*genetics
MH  - Humans
MH  - Interferon Inducers/*pharmacology
MH  - Interferon-gamma/*antagonists & inhibitors
MH  - Trypsin Inhibitors/chemistry/pharmacology
MH  - Urokinase-Type Plasminogen Activator/antagonists & inhibitors
EDAT- 1992/07/01 00:00
MHDA- 1992/07/01 00:01
CRDT- 1992/07/01 00:00
PHST- 1992/07/01 00:00 [pubmed]
PHST- 1992/07/01 00:01 [medline]
PHST- 1992/07/01 00:00 [entrez]
AID - S0022-202X(92)90491-L [pii]
AID - 10.1111/1523-1747.ep12611402 [doi]
PST - ppublish
SO  - J Invest Dermatol. 1992 Jul;99(1):35-9. doi: 10.1111/1523-1747.ep12611402.