title: The antigen presentation function of bone marrow-derived mast cells is spatiotemporally restricted to a subset expressing high levels of cell surface FcepsilonRI and MHC II.
abstract: BACKGROUND
  At present, it is highly controversial whether pure mast cells can serve as antigen presenting cells, and it is not known whether the capacity of antigen presenting function is temporally restricted to a particular subset of differentiated mast cells. Evidence is presented for a novel surface FcepsilonRIhi , MHC II +, and c-kit + pure mast cell subset, temporally restricted as antigen-presenting cells in the immune axis of T-cell activation.
  
  
  RESULTS
  Bone marrow-derived mast cells (BMMC) cultured in the presence of IL-3 for three weeks are pure mast cells based on surface expression of lineage-specific marker, c-kit and FcepsilonRI. Herein we present the first demonstration that approximately 98.7% c-kit + and FcepsilonRI expressing BMMC, further depleted of any contaminated professional antigen-presenting cells, are still fully capable of presenting antigens, i.e., OVA protein, OVA peptide, and IgE-TNP-OVA, to OVA peptide-specific T-cell hybridomas. Notably, IgE-dependent antigen presentation is more efficient compared to that resulting from direct antigen uptake. Importantly, we present the novel finding that only surface FcepsilonRIhi mast cells, also expressing surface MHC II exhibited antigen-presenting function. In contrast, surface FcepsilonRIlo mast cells without expressing surface MHC II were not capable of antigen presentation. Interestingly, the antigen-presenting function of BMMC was irrevocably lost during the third and fourth week in IL-3 or SCF containing cultures.
  
  
  CONCLUSIONS
  This is the first observation to attribute a spatiotemporally restricted antigen-presenting function to a subset of three-week old pure BMMC expressing both high levels of surface FcepsilonRI and surface MHC II. We propose that mast cells play an important role in immune deviating and/or sustaining the activation of infiltrating CD4 T-cells, and modulating T-cell mediated allergic inflammation via its flexibility to present antigens and antigen-IgE complexes.
authors.affiliation: Department of Allergy and Immunology, IgE Therapeutics, Inc., San Diego, CA, USA.
authors.forename: Jian
authors.initials: J
authors.lastname: Gong
authors.forename: Ning-Sun
authors.initials: NS
authors.lastname: Yang
authors.forename: Michael
authors.initials: M
authors.lastname: Croft
authors.forename: I-Chun
authors.initials: IC
authors.lastname: Weng
authors.forename: Liangwu
authors.initials: L
authors.lastname: Sun
authors.forename: Fu-Tong
authors.initials: FT
authors.lastname: Liu
authors.forename: Swey-Shen
authors.initials: SS
authors.lastname: Chen
mesh_terms: D000818:Animals; D017951:Antigen Presentation / Q000276:immunology*; D000938:Antigen-Presenting Cells / Q000276:immunology; D000941:Antigens / Q000276:immunology; D001854:Bone Marrow Cells / Q000166:cytology* / Q000276:immunology*; D002478:Cells, Cultured; D005260:Female; D000949:Histocompatibility Antigens Class II / Q000276:immunology*; D042541:Intracellular Space / Q000378:metabolism; D008407:Mast Cells / Q000166:cytology / Q000276:immunology*; D051379:Mice; D017455:Receptors, IgE / Q000276:immunology*; D013997:Time Factors
chemical_list: D000941:Antigens; D000949:Histocompatibility Antigens Class II; D017455:Receptors, IgE