Stress-free T-cell development: Glucocorticoids are not obligatory

Immunology Today

Volumn 21, Issue 12, 2000, Pages 606-611

  Godfrey, Dale I ^a   Purton, Jared F ^a,b   Boyd, Richard L ^a   Cole, Timothy J ^b  

^a MONASH UNIVERSITY MEDICAL SCHOOL   (Australia)

^b BAKER IDI HEART AND DIABETES INSTITUTE   (Australia)

Author keywords

[No Author keywords available]

Indexed keywords

GLUCOCORTICOID;

ANIMAL CELL; APOPTOSIS; GENE EXPRESSION REGULATION; GENE TARGETING; IMMUNOREGULATION; KNOCKOUT MOUSE; MAJOR HISTOCOMPATIBILITY COMPLEX; MOUSE; NONHUMAN; PRIORITY JOURNAL; PROTEIN DOMAIN; REVIEW; T LYMPHOCYTE ACTIVATION; THYMOCYTE; TRANSACTIVATION;

EID: 0034509630     PISSN: 01675699     EISSN: None     Source Type: Journal    
DOI: 10.1016/S0167-5699(00)01741-2     Document Type: Note

References (29)

1. Steroid hormone receptors: Many actors in search of a plot
2. Molecular mechanisms of anti-inflammatory action of glucocorticoids
3. Crosstalk pathway for inhibition of glucocorticoid-induced apoptosis by T cell receptor signaling
4. Programmed T lymphocyte death. Cell activation- and steroid-induced pathways are mutually antagonistic
5. Rescue of thymocytes and T cell hybridomas from glucocorticoid-induced apoptosis by stimulation via the T cell receptor/CD3 complex: A possible in vitro model for positive selection of the T cell repertoire
6. Steroid production in the thymus: Implications for thymocyte selection
7. A targeted glucocorticoid receptor antisense transgene increases thymocyte apoptosis and alters thymocyte development
8. Thymus-derived glucocorticoids regulate antigen-specific positive selection
9. Thymus-derived glucocorticoids set the thresholds for thymocyte selection by inhibiting TCR-mediated thymocyte activation
10. Glucocorticoids in T-cell development and function
11. Impaired type II glucocorticoid-receptor function in mice bearing antisense RNA transgene
12. Disruption of hypothalamic-pituitary-adrenocortical system in transgenic mice expressing type II glucocorticoid receptor antisense ribonucleic acid permanently impairs T cell function: Effects on T cell trafficking and T cell responsiveness during postnatal development
13. Partial blockade of T-cell differentiation during ontogeny and marked alterations of the thymic microenvironment in transgenic mice with impaired glucocorticoid receptor function
14. Early maturation of T-cell progenitors in the absence of glucocorticoids
15. DNA binding of the glucocorticoid receptor is not essential for survival
16. Specialized ability of thymic epithelial cells to mediate positive selection does not require expression of the steroidogenic enzyme P450scc
17. Targeted disruption of the glucocorticoid receptor gene blocks adrenergic chromaffin cell development and severely retards lung maturation
18. Intrathymic T-cell development and selection proceeds normally in the absence of glucocorticoid receptor signaling
19. + thymocytes in vivo by anti-CD3 or 5′-(N-ethyl)-carboxamide adenosine is blocked by glucocorticoid receptor antagonist RU-486
20. Inhibition of I-Ad-, but not Db-restricted peptide-induced thymic apoptosis by glucocorticoid receptor antagonist RU486 in T cell receptor transgenic mice
21. Progesterone receptors in the thymus are required for thymic involution during pregnancy and for normal fertility
22. Newly generated thymocytes are not refractory to deletion when the α/β component of the T cell receptor is engaged by the superantigen staphylococcal enterotoxin B
23. Several different cell surface molecules control negative selection of medullary thymocytes
24. Paracrine glucocorticoid activity produced by mouse thymic epithelial cells
25. Plasma deoxycorticosterone in man
26. Glucocorticoid production in the murine thymus
27. Cross-talk between the T cell antigen receptor and the glucocorticoid receptor regulates thymocyte development
28. Thymocyte glucocorticoid resistance alters positive selection and inhibits autoimmunity and lymphoproliferative disease in MRL-1pr/1pr mice
29. Thymocyte resistance to glucocorticoids leads to antigen-specific unresponsiveness due to 'holes' in the T cell repertoire