Effects of interleukin-2 on the expression of corticotropin-releasing hormone in nerves and lymphoid cells in secondary lymphoid organs from the Fischer 344 rat

2001 ◽  
Vol 119 (1) ◽  
pp. 37-50 ◽  
Author(s):  
Denise L. Bellinger ◽  
David L. Felten ◽  
Dianne Lorton ◽  
Sabine Brouxhon
Life Sciences ◽  
1995 ◽  
Vol 56 (13) ◽  
pp. 1065-1071 ◽  
Author(s):  
George Mastorakos ◽  
Giovanni Cizza ◽  
Richard Kvetnansky ◽  
Ettore Bergamini ◽  
Marc R Blackman ◽  
...  

2011 ◽  
Vol 233 (1-2) ◽  
pp. 54-64 ◽  
Author(s):  
Srinivasan ThyagaRajan ◽  
Kelley S. Madden ◽  
Brian Teruya ◽  
Suzanne Y. Stevens ◽  
David L. Felten ◽  
...  

1997 ◽  
Vol 185 (5) ◽  
pp. 941-952 ◽  
Author(s):  
Bertrand Dubois ◽  
Béatrice Vanbervliet ◽  
Jérome Fayette ◽  
Catherine Massacrier ◽  
Cees Van Kooten ◽  
...  

After antigen capture, dendritic cells (DC) migrate into T cell–rich areas of secondary lymphoid organs, where they induce T cell activation, that subsequently drives B cell activation. Here, we investigate whether DC, generated in vitro, can directly modulate B cell responses, using CD40L-transfected L cells as surrogate activated T cells. DC, through the production of soluble mediators, stimulated by 3- to 6-fold the proliferation and subsequent recovery of B cells. Furthermore, after CD40 ligation, DC enhanced by 30–300-fold the secretion of IgG and IgA by sIgD− B cells (essentially memory B cells). In the presence of DC, naive sIgD+ B cells produced, in response to interleukin-2, large amounts of IgM. Thus, in addition to activating naive T cells in the extrafollicular areas of secondary lymphoid organs, DC may directly modulate B cell growth and differentiation.


2018 ◽  
Vol 7 (12) ◽  
pp. 1389-1396 ◽  
Author(s):  
Peter Ergang ◽  
Anna Mikulecká ◽  
Martin Vodicˇka ◽  
Karla Vagnerová ◽  
Ivan Mikšík ◽  
...  

Stress is an important risk factors for human diseases. It activates the hypothalamic–pituitary–adrenal (HPA) axis and increases plasma glucocorticoids, which are powerful regulators of immune system. The response of the target cells to glucocorticoids depends not only on the plasma concentrations of cortisol and corticosterone but also on their local metabolism. This metabolism is catalyzed by 11β-hydroxysteroid dehydrogenases type 1 and 2, which interconvert glucocorticoid hormones cortisol and corticosterone and their 11-oxo metabolites cortisone and 11-dehydrocorticosterone. The goal of this study was to determine whether stress modulates glucocorticoid metabolism within lymphoid organs – the structures where immune cells undergo development and activation. Using the resident-intruder paradigm, we studied the effect of social stress on glucocorticoid metabolism in primary and secondary lymphoid organs of Fisher 344 (F344) and Lewis (LEW) rats, which exhibit marked differences in their HPA axis response to social stressors and inflammation. We show that repeated social defeat increased the regeneration of corticosterone from 11-dehydrocorticosterone in the thymus, spleen and mesenteric lymphatic nodes (MLN). Compared with the F344 strain, LEW rats showed higher corticosterone regeneration in splenocytes of unstressed rats and in thymic and MLN mobile cells after stress but corticosterone regeneration in the stroma of all lymphoid organs was similar in both strains. Inactivation of corticosterone to 11-dehydrocorticosterone was found only in the stroma of lymphoid organs but not in mobile lymphoid cells and was not upregulated by stress. Together, our findings demonstrate the tissue- and strain-dependent regeneration of glucocorticoids following social stress.


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