möglich sobald  bei der ZB eingereicht worden ist.
		
    Gene profiling reveals unknown enhancing and suppressive actions of glucocorticoids on immune cells.
        
        FASEB J. 16, 61-71 (2002)
    
    
    
				Glucocorticoids continue to be the major immunomodulatory agents used in clinical medicine today. However, their actions as anti-inflammatory and immunosuppressive drugs are both beneficial and deleterious. We analyzed the effect of glucocorticoids on the gene expression profile of peripheral blood mononuclear cells from healthy donors. DNA microarray analysis combined with quantitative TaqMan PCR and flow cytometry revealed that glucocorticoids induced the expression of chemokine, cytokine, and complement family members as well as of newly discovered innate immune-related genes, including scavenger and Toll-like receptors. In contrast, glucocorticoids repressed the expression of adaptive immune-related genes. Simultaneous inhibitory and stimulatory effects of glucocorticoids were found on inflammatory T helper subsets and apoptosis-related gene clusters. In cells activated by T cell receptor cross-linking, glucocorticoids down-regulated the expression of specific genes that were previously up-regulated in resting cells, suggesting a potential new mechanism by which they exert positive and negative effects. Considering the broad and continuously renewed interest in glucocorticoid therapy, the profiles we describe here will be useful in designing more specific and efficient treatment strategies.
			
			
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        Publikationstyp
        Artikel: Journalartikel
    
 
    
        Dokumenttyp
        Wissenschaftlicher Artikel
    
 
     
    
     
     
    
    
        Sprache
        englisch
    
 
    
        Veröffentlichungsjahr
        2002
    
 
     
    
        HGF-Berichtsjahr
        0
    
 
    
    
        ISSN (print) / ISBN
        0892-6638
    
 
    
        e-ISSN
        1530-6860
    
 
     
     
     
	     
	 
	 
    
        Zeitschrift
        FASEB Journal
    
 
		
    
        Quellenangaben
        
	    Band: 16,  
	    Heft: 1,  
	    Seiten: 61-71 
	    
	    
	
    
 
  
         
        
            Verlag
            Wiley
        
 
        
            Verlagsort
            Bethesda, Md.
        
 
	
         
         
         
         
         
	
         
         
         
    
         
         
         
         
         
         
         
    
        Begutachtungsstatus
        Peer reviewed
    
 
    
        Institut(e)
        Institute of Pancreatic Islet Research (IPI)
    
 
     
     
     
     
     	
    
        PubMed ID
        11772937
    
    
    
        Erfassungsdatum
        2002-12-31