scholarly journals “Alternatively Activated” Dendritic Cells Preferentially Secrete IL-10, Expand Foxp3+CD4+ T Cells, and Induce Long-Term Organ Allograft Survival in Combination with CTLA4-Ig

2006 ◽  
Vol 177 (9) ◽  
pp. 5868-5877 ◽  
Author(s):  
Yuk Yuen Lan ◽  
Zhiliang Wang ◽  
Giorgio Raimondi ◽  
Wenhan Wu ◽  
Bridget L. Colvin ◽  
...  
2008 ◽  
Vol 84 (1) ◽  
pp. 124-133 ◽  
Author(s):  
Amy E. Anderson ◽  
Bethan L. Sayers ◽  
Muzlifah A. Haniffa ◽  
David J. Swan ◽  
Julie Diboll ◽  
...  

2012 ◽  
Vol 45 (1) ◽  
pp. 33-43 ◽  
Author(s):  
Thomas Simon ◽  
Séverine Tanguy-Royer ◽  
Pierre-Joseph Royer ◽  
Nicolas Boisgerault ◽  
Jihane Frikeche ◽  
...  

Blood ◽  
2003 ◽  
Vol 101 (8) ◽  
pp. 3325-3333 ◽  
Author(s):  
Cécile Guillot ◽  
Séverine Ménoret ◽  
Carole Guillonneau ◽  
Cécile Braudeau ◽  
Maria G. Castro ◽  
...  

Abstract Costimulatory blockade using cytotoxic T lymphocyte–associated antigen 4 immunoglobulin (CTLA4Ig) efficiently down-regulates immune responses in animal models and is currently used in autoimmune and transplantation clinical trials, but the precise cellular and molecular mechanisms involved remain unclear. Rats that received allogeneic heart transplants and were treated with adenoviruses coding for CTLA4Ig show long-term allograft survival. The immune mechanisms regulating induction of long-term allograft acceptance were analyzed in splenocytes using mixed leukocyte reactions (MLRs). MLRs of splenocytes but not purified T cells from CTLA4Ig-treated rats showed higher than 75% inhibition compared with controls. Splenocytes from CTLA4Ig-treated rats inhibited proliferation of naive and allogeneically primed splenocytes or T cells. MLR suppression was dependent on soluble secreted product(s). Production of soluble inhibitory product(s) was triggered by a donor antigen-specific stimulation and inhibited proliferation in an antigen-nonspecific manner. CTLA4Ig levels in the culture supernatant were undetectable and neither interleukin-10 (IL-10), transforming growth factor β1 (TGFβ1), IL-4, nor IL-13 were responsible for suppression of MLRs. Inhibition of nitrous oxide (NO) production or addition of IL-2 could not restore proliferation independently, but the combined treatment synergistically induced proliferation comparable with controls. Stimulation of APCs using tumor necrosis factor (TNF)–related activation-induced cytokine (TRANCE) or CD40L and addition of IL-2 normalized MLRs of CTLA4Ig-treated splenocytes. Finally, dendritic cells (DCs), but not T cells, from CTLA4Ig-treated rats inhibited naive MLRs. Altogether, these results provide evidence that after in vivo CTLA4Ig treatment, splenocytes, and in particular DCs, can inhibit alloantigen-induced proliferative responses through secretion of inhibitory products, thus promoting alloantigen-specific tolerance in vivo.


2008 ◽  
Vol 180 (10) ◽  
pp. 6593-6603 ◽  
Author(s):  
Min Hu ◽  
Debbie Watson ◽  
Geoff Y. Zhang ◽  
Nicole Graf ◽  
Yuan M. Wang ◽  
...  

2021 ◽  
Vol 147 (2) ◽  
pp. AB174
Author(s):  
Takao Kobayashi ◽  
Koji Iijima ◽  
Jyoti Lama ◽  
Hirohito Kita

2021 ◽  
Vol 12 (1) ◽  
Author(s):  
Jake W. Rhodes ◽  
Rachel A. Botting ◽  
Kirstie M. Bertram ◽  
Erica E. Vine ◽  
Hafsa Rana ◽  
...  

AbstractTissue mononuclear phagocytes (MNP) are specialised in pathogen detection and antigen presentation. As such they deliver HIV to its primary target cells; CD4 T cells. Most MNP HIV transmission studies have focused on epithelial MNPs. However, as mucosal trauma and inflammation are now known to be strongly associated with HIV transmission, here we examine the role of sub-epithelial MNPs which are present in a diverse array of subsets. We show that HIV can penetrate the epithelial surface to interact with sub-epithelial resident MNPs in anogenital explants and define the full array of subsets that are present in the human anogenital and colorectal tissues that HIV may encounter during sexual transmission. In doing so we identify two subsets that preferentially take up HIV, become infected and transmit the virus to CD4 T cells; CD14+CD1c+ monocyte-derived dendritic cells and langerin-expressing conventional dendritic cells 2 (cDC2).


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