scholarly journals Placental growth factor down-regulates type 1 T helper immune response by modulating the function of dendritic cells

2007 ◽  
Vol 82 (6) ◽  
pp. 1473-1480 ◽  
Author(s):  
Y.-L. Lin ◽  
Y.-C. Liang ◽  
B.-L. Chiang
2006 ◽  
Vol 8 (3) ◽  
pp. 714-720 ◽  
Author(s):  
Clara Maria Ausiello ◽  
Giorgio Fedele ◽  
Raffaella Palazzo ◽  
Fabiana Spensieri ◽  
Alessandra Ciervo ◽  
...  

2009 ◽  
Vol 68 (3) ◽  
pp. 300-304 ◽  
Author(s):  
A Tournadre ◽  
P Miossec

This review focuses on the contribution of the local production of chemokines and cytokines and of dendritic cells (DC) to the pathogenesis of inflammatory myopathies. DC are the most efficient professional antigen-presenting cells (APC), which are critical for the development of innate and adaptive immune responses. Chemokines are important mediators of the immune response as they regulate leucocyte recruitment to tissue and play a key role in inflammatory diseases by acting on T-cell and DC migration. Recent advances indicate that the muscle cell itself could participate in the inflammatory process. Furthermore, the T-helper (Th) type 1 and Th17 proinflammatory cytokines, present in myositis samples, are associated with the migration, differentiation and maturation of inflammatory cells and allow a network of interactions between all the components of the immune response. An understanding of such interactions is essential because it can lead to therapeutic applications.


Blood ◽  
2003 ◽  
Vol 102 (1) ◽  
pp. 36-42 ◽  
Author(s):  
Michel Gilliet ◽  
Martin Kleinhans ◽  
Erica Lantelme ◽  
Dirk Schadendorf ◽  
Günter Burg ◽  
...  

Abstract Dendritic cells (DCs) represent the most potent antigen-presenting cells of the immune system capable of initiating primary immune responses to neoantigens. Here we characterize the primary CD4 T-cell immune response to protein keyhole limpet hemocyanin (KLH) in 5 metastatic melanoma patients undergoing a tumor peptide–based dendritic cell vaccination trial. Monocyte-derived dendritic cells displaying a semimature phenotype, as defined by surface markers, were loaded ex vivo with antigen and injected intranodally at weekly intervals for 4 weeks. All patients developed a strong and long-lasting delayed-type hypersensitivity reactivity to KLH, which correlated with the induction of KLH-dependent proliferation of CD4 T cells in vitro. Secondary in vitro stimulation with KLH showed significant increase in interferon-γ and interleukin-2 (IL-2) but not IL-4, IL-5, nor IL-10 secretion by bulk T cells. On the single-cell level, most TH1 cells among in vitro–generated KLH-specific T-cell lines confirmed the preferential induction of a KLH-specific type 1 T helper immune response. Furthermore, the induction of KLH-specific antibodies of the IgG2 subtype may reflect the induction of a type 1 cytokine profile in vivo after vaccination. Our results indicate that intranodal vaccination with semimature DCs can prime strong, long-lasting CD4 T-cell responses with a TH1-type cytokine profile in cancer patients. (Blood. 2003;102:36-42)


2008 ◽  
Vol 89 (9) ◽  
pp. 2228-2239 ◽  
Author(s):  
Ian B. Hogue ◽  
Seema H. Bajaria ◽  
Beth A. Fallert ◽  
Shulin Qin ◽  
Todd A. Reinhart ◽  
...  

Many aspects of the complex interaction between human immunodeficiency virus type 1 (HIV-1) and the human immune system remain elusive. Our objective was to study these interactions, focusing on the specific roles of dendritic cells (DCs). DCs enhance HIV-1 infection processes as well as promote an antiviral immune response. We explored the implications of these dual roles. A mathematical model describing the dynamics of HIV-1, CD4+ and CD8+ T-cells, and DCs interacting in a human lymph node was analysed and is presented here. We have validated the behaviour of our model against non-human primate simian immunodeficiency virus experimental data and published human HIV-1 data. Our model qualitatively and quantitatively recapitulates clinical HIV-1 infection dynamics. We have performed sensitivity analyses on the model to determine which mechanisms strongly affect infection dynamics. Sensitivity analysis identifies system interactions that contribute to infection progression, including DC-related mechanisms. We have compared DC-dependent and -independent routes of CD4+ T-cell infection. The model predicted that simultaneous priming and infection of T cells by DCs drives early infection dynamics when activated T-helper cell numbers are low. Further, our model predicted that, while direct failure of DC function and an indirect failure due to loss of CD4+ T-helper cells are both significant contributors to infection dynamics, the former has a more significant impact on HIV-1 immunopathogenesis.


Cytokine ◽  
2010 ◽  
Vol 52 (1-2) ◽  
pp. 82
Author(s):  
Aurelio Flores-Garcı´a ◽  
Vicente Garibaldi-Becerra ◽  
Martha Barba-Barajas ◽  
Jesus S. Velarde-Félix ◽  
Luis E. Wong-Ley-Madero ◽  
...  

1996 ◽  
Vol 183 (6) ◽  
pp. 2669-2674 ◽  
Author(s):  
F Powrie ◽  
J Carlino ◽  
M W Leach ◽  
S Mauze ◽  
R L Coffman

A T helper type 1 (Th1)-mediated colitis with similarities to inflammatory bowel disease in humans developed in severe combined immunodeficiency mice reconstituted with CD45RB(high) CD4+ splenic T cells and could be prevented by cotransfer of CD45RB(low) CD4+ T cells. Inhibition of this Th1 response by the CD45RB(low) T cell population could be reversed in vivo by an anti-transforming growth factor (TGF) beta antibody. Interleukin (IL) 4 was not required for either the differentiation of function of protective cells as CD45RB(low) CD4+ cells from IL-4-deficient mice were fully effective. These results identify a subpopulation of peripheral CD4+ cells and TGF-beta as critical components of the natural immune regulatory mechanism, which prevents the development of pathogenic Th1 responses in the gut, and suggests that this immunoregulatory population is distinct from Th2 cells.


2004 ◽  
Vol 5 (9) ◽  
pp. 909-918 ◽  
Author(s):  
Till A Röhn ◽  
Marianne Boes ◽  
Dirk Wolters ◽  
Sebastian Spindeldreher ◽  
Bernd Müller ◽  
...  
Keyword(s):  
T Helper ◽  

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