T cell subpopulation regulating gut immunity

Chemistry: molecular biology and microbiology – Measuring or testing process involving enzymes or... – Involving antigen-antibody binding – specific binding protein...

Reexamination Certificate

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C435S006120, C435S007200, C435S007240, C435S007800, C435S029000, C436S501000

Reexamination Certificate

active

07829289

ABSTRACT:
The invention relates to methods of modulating an immune response in a mammal by modulating the activity of Jα33 T cells or of MR1 polypeptide in vitro, ex vivo or in vivo. The invention also relates to methods of regulating the activity of immune cells, particularly of T lymphocytes and/or B lymphocytes by regulating the activity of MR1 in vitro, ex vivo or in vivo. The invention further comprises methods of screening active compounds using MR1 or fragments thereof, or nucleic acid encoding the same, or recombinant host cells expressing said polypeptide. The invention also deals with a pharmaceutical composition comprising Jα33 T cells, MR1 polypeptide or a compound that modulates the activity of Jα33 TCR T cells or of MR1 polypeptide and a pharmaceutically acceptable vehicle or carrier. The invention further deals with methods of diagnosis for intestinal diseases related to a defect of the activity of said Jα33 T cells or MR1 polypeptide.

REFERENCES:
patent: 2003/0215808 (2003-11-01), Lantz et al.
Treiner et al, “The phylogenetically conserved Vα19-Jα33 T cell subpopulation: selection , localization and ligand recognition” Abstract SFI Nov. 2001 SFI—Annual Congress of the French Society of Immunology, Paris, Nov. 21-23, 2001.
Treiner et al, “The phylogenetically conserved Vα19-Jα33 T cell subpopulation: selection, localization and ligand recognition”, Keystone Symposia—“Innate Immunity : Evolution and link to adaptive immunity”, Feb. 3-9, 2002, Taos NM.
Riegert et al “Genomics, Isoforms, Expression, and Phylogeny of the MHC Class I-related MR1 Gene” The Journal of Immunology, 1998, 161:4066-4077.
Badr-el-Din et al, “Local immunity in ulcerative colitis: evidence for defective secretory IgA production”, Gut. 1988, August; 29(8):1070-5 (Abstract).
Cicalese et al, “Decreased mucosal IgA levels in ileum of patients with chronic ulcerative colitis”, Dig Dis Sci. Apr. 1995; 40(4):805-11 (Abstract).
Marteau et al, “Immunological study of histologically non-involved jejunum during Crohn's disease: evidence for reduced in vivo secretion of secretory IgA”, Clin Exp Immunol. May 1990; 80(2):196-201 (Abstract).
Mestecky et al., “Intestinal IgA: novel views on its function in the defence of the largest mucosal surface”, Gut, 1999, 44:2-5.
Stevceva et al, “the inflammatory infiltrate in the acute stage of the dextran sulphate sodium induced colitis: B cell response differs depending on the percentage of DSS used to induct it”, BMC Clinical Pathology, 2001, 1:3.
Definition—Inflammatory Bowel Disease—MeSH—NCBI web site—printed Mar. 17, 2007.

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