title: Induction of a proliferative response of T cells by a high-molecular antigen in Dermatophagoides farinae feces.
abstract: BACKGROUND
  We have previously demonstrated that high-molecular mite antigen (HM1) from Dermatophagoides farinae feces is an allergen which binds to mite-allergic patients IgE. HM1 also induced a proliferative response in lymph node cells from mite-immunized mice as well as nonimmunized mice. In the present study, we demonstrated that HM1 induced T cell proliferation and investigated the HM1-stimulated T cell proliferative pathways using nonallergic human peripheral blood mononuclear cells (PMBC).
  
  
  METHODS
  Blood samples were obtained from 10 healthy donors. Using primary culture, T cell response stimulated with HM1 was performed on purified T cells, CD19+ cell-depleted PBMC and CD11b+ cell-depleted PBMC. In addition, interleukin (IL)-5 and interferon (IFN)-gamma produced by mite-allergic and healthy donors stimulated with HM1 were estimated by enzyme immunoassay.
  
  
  RESULTS
  T cell proliferation was detected only in CD19+ cell-depleted PBMC. When T cells were cocultured with CD11b+ cells they recovered their proliferative response to HM1. In addition, the pathway of HM1-stimulated T cell proliferation did not involve HLA class II restriction. Both activated CD11b+ cells and their conditioned media were needed to induce HM1-stimulated T cell proliferation. Furthermore, HM1 induced IFN-gamma production in both healthy and allergic donors.
  
  
  CONCLUSIONS
  The high-molecular mite antigen, HM1, induced a proliferative response of T cells in healthy as well as allergic donors, without HLA class II restriction. Our results suggest that further investigation of HM1 could constitute a valuable avenue of research into complex allergic diseases.
authors.affiliation: Department of Molecular Biotechnology, Graduate School of Advanced Sciences of Matter, Hiroshima University, Kagamiyama 1-4-1, Higashi-Hiroshima 739-8527, Japan. lovero@hiroshima-u.ac.jp
authors.forename: Airo
authors.initials: A
authors.lastname: Tategaki
authors.forename: Seiji
authors.initials: S
authors.lastname: Kawamoto
authors.forename: Kanako
authors.initials: K
authors.lastname: Hashimoto
authors.forename: Takahide
authors.initials: T
authors.lastname: Okuda
authors.forename: Tsunehiro
authors.initials: T
authors.lastname: Aki
authors.forename: Osamu
authors.initials: O
authors.lastname: Suzuki
authors.forename: Kazuhisa
authors.initials: K
authors.lastname: Ono
authors.forename: Seiko
authors.initials: S
authors.lastname: Shigeta
mesh_terms: D000911:Antibodies, Monoclonal / Q000276:immunology; D039741:Antigens, Dermatophagoides; D018845:CD11 Antigens / Q000276:immunology; D002455:Cell Division / Q000276:immunology; D004797:Enzyme-Linked Immunosorbent Assay; D005243:Feces; D005434:Flow Cytometry; D006023:Glycoproteins / Q000276:immunology*; D000949:Histocompatibility Antigens Class II / Q000276:immunology; D006801:Humans; D006967:Hypersensitivity / Q000276:immunology; D018189:Immunomagnetic Separation; D007371:Interferon-gamma / Q000096:biosynthesis; D015848:Interleukin-5 / Q000096:biosynthesis; D008213:Lymphocyte Activation / Q000276:immunology; D008970:Molecular Weight; D013601:T-Lymphocytes / Q000276:immunology* / Q000378:metabolism
chemical_list: D000911:Antibodies, Monoclonal; D039741:Antigens, Dermatophagoides; D018845:CD11 Antigens; D006023:Glycoproteins; D000949:Histocompatibility Antigens Class II; D015848:Interleukin-5; D007371:Interferon-gamma