Oral tolerance to food-induced systemic anaphylaxis mediated by the C-type lectin SIGNR1
Oral tolerance to food-induced systemic anaphylaxis mediated by the C-type lectin SIGNR1
Yufeng Zhou , et al . 2010. Nat Med. 10.1038
Speaker: Chia-Lun Tsai(蔡佳倫) Time: 14:10-15:00, Dec. 29, 2010
Commentator: Dr. Chi-Chang Shieh (謝奇璋 醫師) Place: Room 601
Abstract
Gastrointestinal laminar propria dendritic cells (LPDCs) can use innate pattern-recognition molecule such as the C-type lectin receptors (CLRs) SIGNR1 to recognize complex glycan structures of pathogens via its C-type (calcium dependent) carbohydrate-recognition domains (CRDs) forendocytosis of pathogens. The authors hypothesis that the sugar-modified antigen Man51-BSA , which is similar to mannosylated stuctures of pathogen ligand, may target LPDC C-type lectin receptors (CLRs) SIGNR1 to induce oral tolerance in food-induced systemic anaphylaxis . The authors found BSA-sensitized mice pretreated with Man51-BSA , but not with BSA , was able to decrease the severity of anaphylaxis after challenged with BSA in this murine model of food-induced anaphylaxis . To analysis the role of LPDC in this murine model of glycosylated BSA-induced anaphylaxis, naive mice were treated with oral FITC-labeled Man51-BSA or FITC-labeled BSA. It was found that LPDCs (CLRs) SIGNR1 can be selected in the CD11c+CD11b+ DC subset that bound with FITC-labeled Man51-BSA or FITC-labeled BSA in flow cytometry analyses. To examine the cytokines production in lamina propria CD11c+ DCs stimulated with BSA or Man51-BSA, T cells cultured with Man51-BSA-pulsed or BSA-pulsed LPDCs, and there was a significantly increased concentrations of IL-10 and IFN-γ in Man51-BSA co-culture condition.
References
1. Teunis B. H. Geijtenbeek, Anneke Engering, and Yvette van Kooyk DC-SIGN, a C-type lectin on dendritic cells that unveils manyaspects of dendritic cell biology Journal of Leukocyte Biology Volume 71, June 2002 921.
2. Mowat, A.M. Anatomical basis of tolerance and immunity to intestinal antigens. Nat. Rev. Immunol. 3, 331–341 (2003).