PMID- 8764297
OWN - NLM
STAT- MEDLINE
DCOM- 19960919
LR  - 20171213
IS  - 0002-9513 (Print)
IS  - 0002-9513 (Linking)
VI  - 270
IP  - 6 Pt 2
DP  - 1996 Jun
TI  - 11 beta-hydroxysteroid dehydrogenase modulation of glucocorticoid activities in 
      lymphoid organs.
PG  - R1296-306
AB  - The immunoregulatory effects of glucocorticoids (GCS) are linked to their 
      capacity to alter the production of various species of cytokines associated with 
      immune and inflammatory processes. The present study determined that the 
      influences of GCS within particular lymphoid organs vary, depending on the 
      specific activity of 11 beta-hydroxysteroid dehydrogenase (11 beta-HSD) within 
      the tissue. This enzyme converts active GCS to inactive metabolites and was found 
      to display greater activity in peripheral than in mucosal lymphoid organs. A 
      direct correlation was found between 11 beta-HSD activity and the preferential 
      production of type 1 cytokines by T-cells residing within certain lymphoid 
      organs. It was established that lymphoid organ 11 beta-HSD was localized in the 
      immobile stromal cell components. Inhibition of 11 beta-HSD activity in vivo 
      reduced type 1 and enhanced type 2 cytokine production by activated T-cells, and 
      it also depressed the ability of animals to generate contact hypersensitivity 
      responses. We conclude that GCS levels can be controlled within lymphoid organs 
      through oxidative inactivation by 11 beta-HSD. GCS action is, therefore, 
      dependent on tissue levels of 11 beta-HSD activity, the number of GCS receptors 
      in a responsive cell, and the concentration of circulating GCS.
FAU - Hennebold, J D
AU  - Hennebold JD
AD  - Department of Pathology, University of Utah School of Medicine, Salt Lake City 
      84132, USA.
FAU - Ryu, S Y
AU  - Ryu SY
FAU - Mu, H H
AU  - Mu HH
FAU - Galbraith, A
AU  - Galbraith A
FAU - Daynes, R A
AU  - Daynes RA
LA  - eng
GR  - AG-11475/AG/NIA NIH HHS/United States
GR  - CA-25917/CA/NCI NIH HHS/United States
PT  - Journal Article
PT  - Research Support, U.S. Gov't, Non-P.H.S.
PT  - Research Support, U.S. Gov't, P.H.S.
PL  - United States
TA  - Am J Physiol
JT  - The American journal of physiology
JID - 0370511
RN  - 0 (Cytokines)
RN  - 0 (Glucocorticoids)
RN  - 0 (Isoenzymes)
RN  - EC 1.1.- (Hydroxysteroid Dehydrogenases)
RN  - EC 1.1.1.146 (11-beta-Hydroxysteroid Dehydrogenases)
SB  - IM
MH  - 11-beta-Hydroxysteroid Dehydrogenases
MH  - Animals
MH  - Cytokines/biosynthesis
MH  - Female
MH  - Glucocorticoids/*metabolism
MH  - Hydroxysteroid Dehydrogenases/*physiology
MH  - Isoenzymes/metabolism
MH  - Liver/enzymology
MH  - Lymphocyte Activation
MH  - Lymphoid Tissue/*enzymology
MH  - Mice
MH  - Mice, Inbred C3H
MH  - Stromal Cells/enzymology
MH  - T-Lymphocytes/metabolism/physiology
EDAT- 1996/06/01 00:00
MHDA- 1996/06/01 00:01
CRDT- 1996/06/01 00:00
PHST- 1996/06/01 00:00 [pubmed]
PHST- 1996/06/01 00:01 [medline]
PHST- 1996/06/01 00:00 [entrez]
AID - 10.1152/ajpregu.1996.270.6.R1296 [doi]
PST - ppublish
SO  - Am J Physiol. 1996 Jun;270(6 Pt 2):R1296-306. doi: 
      10.1152/ajpregu.1996.270.6.R1296.