Prolactin enhances production of interferon-γ, interleukin-12, and interleukin-10, but not of tumor necrosis factor-α, in a stimulus-specific manner

Cytokine ◽  
2003 ◽  
Vol 21 (4) ◽  
pp. 187-194 ◽  
Author(s):  
Khalid Z. Matalka
1998 ◽  
Vol 178 (4) ◽  
pp. 1095-1104 ◽  
Author(s):  
Steven M. Holland ◽  
Susan E. Dorman ◽  
Annette Kwon ◽  
Ian F. Pitha‐Rowe ◽  
David M. Frucht ◽  
...  

2010 ◽  
Vol 37 (8) ◽  
pp. 1596-1606 ◽  
Author(s):  
HONGYAN AN ◽  
VASUDHA CHANDRA ◽  
BARBARA PIRAINO ◽  
LUIS BORGES ◽  
CAROLYN GECZY ◽  
...  

Objective.Leukocyte immunoglobulin-like receptor A3 (LILRA3) belongs to a family of cell-surface receptors with inhibitory or activating functions. LILRA3 lacks transmembrane and cytoplasmic domains, suggesting that it may be secreted. LILRA3 has high homology to activating LILRA1 and A2, hence may act as a soluble agonist/antagonist to these receptors. Individuals lacking the LILRA3 gene have higher incidence of multiple sclerosis and Sjögren’s syndrome, suggesting LILRA3 may be antiinflammatory. LILRA3 mRNA was detected in monocytes and mast cells but no protein expression has ever been described. Our aim was to examine LILRA3 protein expression in serum and synovial fluid of patients with rheumatoid arthritis (RA) and determine its in vitro regulation.Methods.We developed a new ELISA to examine levels of LILRA3 in serum, synovial fluid, and/or culture supernatants from controls and patients with RA, degenerative arthritis, or gout. We used qRT-PCR and flow cytometry to determine the expression and cytokine-mediated regulation of LILRA3.Results.LILRA3 protein is constitutively present in normal serum, with significantly higher concentrations in patients with RA. Serum LILRA3 concentrations from RA patients correlated with disease activity and levels in synovial fluid. Treatment of monocytes with interleukin 10 or interferon-γ significantly upregulated while tumor necrosis factor-α significantly downregulated LILRA3 mRNA and protein expression.Conclusion.We show for the first time that LILRA3 is significantly increased in serum of patients with RA and is tightly regulated by key cytokines involved in pathogenesis of RA. These results suggest that LILRA3 may play a role in chronic inflammatory conditions such as RA.


1993 ◽  
Vol 23 (8) ◽  
pp. 2045-2048 ◽  
Author(s):  
Sally Betz Corradin ◽  
Nicolas Fasel ◽  
Yolande Buchmüller-Rouiller ◽  
Adriana Ransijn ◽  
Josiane Smith ◽  
...  

2011 ◽  
Vol 52 (1) ◽  
pp. 171 ◽  
Author(s):  
Aditi Sen ◽  
Suman Kalyan Paine ◽  
Imran Hussain Chowdhury ◽  
Lakshmi Kanta Mondal ◽  
Amrita Mukherjee ◽  
...  

1996 ◽  
Vol 72 (4) ◽  
pp. 245-252 ◽  
Author(s):  
C. A. M. van Bergen ◽  
W. M. Smit ◽  
D. A. van Sluijters ◽  
M. Rijnbeek ◽  
R. Willemze ◽  
...  

Author(s):  
Michelino Di Rosa ◽  
Maria Musumeci ◽  
Anna Scuto ◽  
Salvatore Musumeci ◽  
Lucia Malaguarnera

AbstractHuman chitotriosidase is a chitinolytic enzyme and mainly produced by activated macrophages. Recently, we observed that prolactin, which is structurally related to several cytokines and is involved in regulating monocyte/macrophage functions, upregulates chitotriosidase gene expression in human macrophages, suggesting that chitotriosidase is not only a biochemical marker of macrophage activation in lysosomal diseases and hematological disorders, but also may reflect induction of an immunological response. To confirm this hypothesis we evaluated by quantitative real-time PCR the mRNA chitotriosidase levels in human monocytes/macrophages following treatment with pro-inflammatory stimuli such as interferon-γ, tumor necrosis factor-α, lipopolysaccharide, and interleukin-10, an anti-inflammatory cytokine. Stimulation of macrophages with interferon-γ, tumor necrosis factor-α and lipopolysaccharide resulted in increased levels of chitotriosidase mRNA, as well as chitotriosidase activity, whereas interleukin-10 decreased chitotriosidase synthesis. This finding is consistent with the hypothesis that the production of chitotriosidase by macrophages could have biological relevance in the immune response.


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