Group leader: This e-mail address is being protected from spambots. You need JavaScript enabled to view it   (Assistant professor, PhD)
Members: Lisa Larsson (PhD-student), Yu Fang (graduate student), Linnea Lidell (project student).

My research interest focuses on the two functioning arms of mast cells, i.e. their classical role in allergy and the more recently appreciated roles in innate and adaptive immunity.

Mast cells are important effector cells in allergic diseases. They express receptors for immunoglobulin molecules and signalling through these Fc receptors mediates the allergic cellular events. We are currently studying the effect of a particular Fc receptor, i.e. FcγRIIb, on mast cell biology. This low affinity receptor binds IgG in the form of antigen-IgG immune-complexes. Co-crosslinking of FcγRIIb with activatory receptors by immune-complexes dampens cellular activation. Therefore FcγRIIb is critical for down-modulating immune responses, providing a mechanism to limit the duration of immune responses that may otherwise lead to allergy. Our aim is to study the effects of the interaction between FcγRIIb and immune-complexes composed of allergen and IgG on the regulation of allergic inflammation as well as therapeutic interventions such as antigen-specific immunotherapy.

More recently, the importance of mast cells has been extended beyond the scope of allergy. They secrete a large spectrum of cytokines and chemokines which play a central role in orchestrating both the innate and adaptive immunity. Mast cell activators are demonstrated to be powerful adjuvants which facilitate humoral immune responses. The mechanism is suggested to involve the inflammatory mediators (e.g. TNF-a) released by mast cells, which in this way promote dendritic cell  maturation and migration. I hypothesize that conventional mucosal adjuvants may also exert their adjuvanticity by activating mast cells, or mast cell activation can be exploited as a novel strategy for designing adjuvants with better potency. Our aim in this project is to design new adjuvant cocktails that may activate mast cells and provide better adjuvanticity.

Important publications

Fang Y, L Larsson, J Mattsson, N Lycke, and Z Xiang, Mast cells contribute to the mucosal adjuvant effect of CTA1DD after IgG-complex formation. J. Immunol. 2010; 185(5):2935-41.

Wang H, Mobini R, Fang Y, Barrenäs F, Zhang H, Xiang Z, Benson M. Allergen-challenge of PBMCs from patients with seasonal allergic rhinitis increases IL-17RB, which regulates basophil apoptosis and degranulation. Clin Exp Allergy. 2010; 40(8):1194-202. 

Brownlie, R.J., K.E. Lawlor, H.A. Niederer, A.J. Cutler, Z. Xiang. M.R. Clatworthy, R.A. Floto, D.R. Greaves, P.A. Lyons, and K.G. Smith. 2008. Distinct cell-specific control of autoimmunity and infection by FcgRIIb. J. Exp. Med. 2008. 205(4):883-95. 

Karlberg M, Xiang Z, Nilsson G. FcgammaRI-Mediated Activation of Human Mast Cells Promotes Survival and Induction of the Pro-survival Gene Bfl-1. J. Clin. Immunol. 2008. 28(3):250-5.

Xiang Z, AJ Cutler, RJ Brownlie, K Fairfax, KE Lawlor, E Severinson, EU Walker, RA Manz, DM Tarlinton, and KGC Smith. FcgRIIb controls bone marrow plasma cell persistence and apoptosis. Nat. Immunol. 2007. 8(4): 419-29.  

Xiang Z, Moller C, Nilsson G. IgE-receptor activation induces survival and Bfl-1 expression in human mast cells but not basophils. Allergy. 2006. 61(9):1040-6.