Ligand and cytokine dependence of the immunosuppressive pathway of tryptophan catabolism in plasmacytoid dendritic cells.

نویسندگان

  • Francesca Fallarino
  • Ciriana Orabona
  • Carmine Vacca
  • Roberta Bianchi
  • Stefania Gizzi
  • Carine Asselin-Paturel
  • Maria Cristina Fioretti
  • Giorgio Trinchieri
  • Ursula Grohmann
  • Paolo Puccetti
چکیده

Murine plasmacytoid dendritic cells (pDCs) have been credited with a unique ability to express indoleamine 2,3-dioxygenase (IDO) function and mediate immunosuppression in specific settings; yet, the conditions of spontaneous versus induced activity have remained unclear. We have used maneuvers known to up-regulate IDO in different cell types and have examined the relative efficacy and mechanisms of the induced activity in splenic pDCs, namely, after specific receptor engagement by CTLA-4-Ig, CD200-Ig or CD28-Ig, the latter in combination with silenced expression of the suppressor of cytokine signaling 3 (SOCS3) gene. We found that pDCs (CD11c+ mPDCA-1+ 120G8+) do not express IDO and are not tolerogenic under basal conditions. B7-1 engagement by CTLA-4-Ig, CD200R1 engagement by CD200-Ig and B7-1/B7-2 engagement by CD28-Ig in SOCS3-deficient pDCs were each capable of initiating IDO-dependent tolerance via different mechanisms. IFN-gamma was the major cytokine responsible for CTLA-4-Ig effects, and type I IFNs for those of CD200-Ig. Immunosuppression by CD28-Ig in the absence of SOCS3 required IFN-gamma induction and IFN-like actions of IL-6. Therefore, although pDCs do not mediate IDO-dependent tolerance constitutively, multiple ligands and cytokines will contribute to the expression of a tolerogenic phenotype by pDCs in the mouse.

برای دانلود رایگان متن کامل این مقاله و بیش از 32 میلیون مقاله دیگر ابتدا ثبت نام کنید

ثبت نام

اگر عضو سایت هستید لطفا وارد حساب کاربری خود شوید

منابع مشابه

Murine plasmacytoid dendritic cells initiate the immunosuppressive pathway of tryptophan catabolism in response to CD200 receptor engagement.

In this study, using a soluble CD200-Ig fusion protein, we provide evidence that murine dendritic cells (DCs) possess a functional CD200R, whose engagement results in the reinforcement or appearance of immunosuppressive properties in these cells. In particular, the plasmacytoid subset (CD11c+B220+120G8+) of splenic DCs (pDCs) is induced by CD200-Ig to express the enzyme IDO, which initiates the...

متن کامل

Cutting edge: silencing suppressor of cytokine signaling 3 expression in dendritic cells turns CD28-Ig from immune adjuvant to suppressant.

CTLA-4-Ig and CD28-Ig are both agonist ligands of B7 coreceptor molecules on mouse dendritic cells (DCs), yet they bias the downstream response in opposite directions, and CTLA-4-Ig promotes tolerance, whereas CD28-Ig favors the onset of immunity. Although B7 engagement by either ligand leads to a mixed cytokine response, a dominant IL-6 production in response to CD28-Ig prevents the IFN-gamma-...

متن کامل

Plasmacytoid dendritic cells in angiolymphoid hyperplasia with eosinophilia

Background: Angiolymphoid hyperplasia with eosinophilia (ALHE) is characterized by irregularly-shaped blood vessels with an inflammatory infiltrate. While absent from normal skin, plasmacytoid dendritic cells (pDCs) infiltrate the skin upon injury and during several infectious, inflammatory, and neoplastic entities. In addition to providing anti-viral resistance, pDCs link the innate and adapti...

متن کامل

P 78: The Role of Kynurenine Pathway in Suicidal Behavior and Depression

According to global statistics, over 80,000 deaths occur by suicide annually. Up to 90% of complete suicides are based on psychiatric disorders specifically major depressive disorder (MDD) and bipolar disorder. Furthermore high levels of inflammation have been indicated in suicidal patients in both central nervous system and the peripheral blood. Two biological mechanisms that play a key role i...

متن کامل

ذخیره در منابع من


  با ذخیره ی این منبع در منابع من، دسترسی به آن را برای استفاده های بعدی آسان تر کنید

عنوان ژورنال:
  • International immunology

دوره 17 11  شماره 

صفحات  -

تاریخ انتشار 2005