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Abstract
The immune system must be tightly controlled not only to guarantee efficient protection from invading pathogens and oncogenic cells but also to avoid exaggerated immune responses and autoimmunity. This is achieved through interactions amongst leukocytes themselves, by signals from stromal cells and also by various hormones, including glucocorticoids. The glucocorticoids are a class of steroid hormones that exert a wide range of anti-inflammatory and immunosuppressive activities after binding to the glucocorticoid receptor. The power of these hormones was acknowledged many decades ago, and today synthetic derivatives are widely used in the treatment of inflammatory disorders, autoimmunity and cancer. In this review, we summarize our present knowledge of the molecular mechanisms of glucocorticoid action, their influence on specific leukocytes and the induction of thymocyte apoptosis, with an emphasis on how molecular genetics has contributed to our growing, although still incomplete, understanding of these processes.
| Abbreviations | ||
| AF | = | Activation function |
| APC | = | Antigen presenting cells |
| Apaf-1 | = | apoptosis protease-activating factor 1 |
| AP-1 | = | transcription factor |
| Bcl-2 | = | family of proteins that control the integrity of the mitochondrial outer membrane |
| Bcl-XL | = | Bcl-2 family member |
| BH3-only proteins | = | one class of pro-apoptotic Bcl-2 family members |
| CAM | = | Cell adhesion molecule |
| CBP/p300 | = | CREB binding protein |
| CD | = | receptors |
| COX-2 | = | Cyclooxygenase-2 |
| Cre | = | Type I topoisomerase from bacteriophage P1 |
| DBD | = | DNA-binding domain |
| DC | = | Dendritic cell |
| Dex | = | Dexamethasone |
| DP | = | Double positive |
| Fas | = | Death receptor CD95 |
| GC | = | Glucocorticoid hormones |
| GILZ | = | Glucocorticoid induced leucine zipper |
| GR | = | Glucocorticoid receptor |
| GRE | = | Gucocorticoid response element |
| IFNγ | = | proinflammatory cytokine |
| IκB-α | = | inhibitor of NF-kB |
| IL | = | interleukin |
| JNK | = | c-Jun N-terminal kinase |
| LBD | = | Ligand binding domain |
| LC | = | Langerhans cell |
| LxxLL | = | Nuclear receptor interaction motif; NR box |
| MHC | = | Major histocompatibility complex |
| NF-κB | = | Nuclear factor κ B |
| NK | = | Natural killer cells |
| NLS | = | Nuclear localisation signals |
| NO | = | Nitrous oxide |
| SP | = | Single positive |
| TCR | = | T cell receptor |
| TNF | = | Tumour necrosis factor. |
| Abbreviations | ||
| AF | = | Activation function |
| APC | = | Antigen presenting cells |
| Apaf-1 | = | apoptosis protease-activating factor 1 |
| AP-1 | = | transcription factor |
| Bcl-2 | = | family of proteins that control the integrity of the mitochondrial outer membrane |
| Bcl-XL | = | Bcl-2 family member |
| BH3-only proteins | = | one class of pro-apoptotic Bcl-2 family members |
| CAM | = | Cell adhesion molecule |
| CBP/p300 | = | CREB binding protein |
| CD | = | receptors |
| COX-2 | = | Cyclooxygenase-2 |
| Cre | = | Type I topoisomerase from bacteriophage P1 |
| DBD | = | DNA-binding domain |
| DC | = | Dendritic cell |
| Dex | = | Dexamethasone |
| DP | = | Double positive |
| Fas | = | Death receptor CD95 |
| GC | = | Glucocorticoid hormones |
| GILZ | = | Glucocorticoid induced leucine zipper |
| GR | = | Glucocorticoid receptor |
| GRE | = | Gucocorticoid response element |
| IFNγ | = | proinflammatory cytokine |
| IκB-α | = | inhibitor of NF-kB |
| IL | = | interleukin |
| JNK | = | c-Jun N-terminal kinase |
| LBD | = | Ligand binding domain |
| LC | = | Langerhans cell |
| LxxLL | = | Nuclear receptor interaction motif; NR box |
| MHC | = | Major histocompatibility complex |
| NF-κB | = | Nuclear factor κ B |
| NK | = | Natural killer cells |
| NLS | = | Nuclear localisation signals |
| NO | = | Nitrous oxide |
| SP | = | Single positive |
| TCR | = | T cell receptor |
| TNF | = | Tumour necrosis factor. |