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An Adoptive Transfer Model of Rheumatoid Arthritis in Mice

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Glucocorticoid receptor: implications for rheumatic diseases.

T Kino¹, E Charmandari, G P Chrousos

¹Eunice Kennedy Shriver National Institute of Child Health and Human Development, National Institutes of Health, Bethesda, MD 20892, USA. kinot@mail.nih.gov

Clinical and Experimental Rheumatology

|October 25, 2011

Summary

This summary is machine-generated.

The glucocorticoid receptor (GR) has two main forms, GRα and GRβ, influencing immune responses and potentially rheumatic diseases. Understanding GR regulation offers therapeutic timing strategies for autoimmune disorders.

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Area of Science:

Molecular biology
Endocrinology
Immunology

Background:

The glucocorticoid receptor (GR) is a key mediator of glucocorticoid effects.
The human GR gene yields two isoforms, GRα and GRβ, through alternative splicing.
GRα binds glucocorticoids and mediates classical actions, while GRβ inhibits GRα activity.

Purpose of the Study:

To elucidate the structure, function, and isoforms of the glucocorticoid receptor.
To explore the role of GR in immune system regulation.
To investigate the potential involvement of GRβ in rheumatic diseases and therapeutic implications of GR circadian regulation.

Main Methods:

Analysis of the human GR gene structure and alternative splicing.
Characterization of GRα and GRβ isoforms and their functions.
Review of genomic and non-genomic GR actions, including immune system regulation.

Main Results:

GRα is the primary glucocorticoid-binding receptor, mediating transcriptional regulation.
GRβ acts as a dominant negative regulator of GRα.
GR exhibits both genomic and rapid non-genomic effects, impacting the immune system.

Conclusions:

GR isoforms play critical roles in immune regulation.
GRβ may be implicated in the pathogenesis of rheumatic diseases.
Circadian regulation of GR activity presents therapeutic opportunities for autoimmune inflammatory disorders.