title: Crohn's disease: innate immunodeficiency?
abstract: In the past, Crohn's disease (CD) has been understood primarily as an immunologic disorder characterized by an abnormal T-cell response. Recent in vitro and in vivo data suggests that CD may instead be precipitated by innate immune dysfunction resulting from a combination of genetic and environmental factors. Some reports have demonstrated a defective immune response in a variety of other cellular components, including neutrophils, monocytes and dendritic cells. Recent studies of granulocyte-macrophage colony-stimulating factor (GM-CSF) in CD, aiming to stimulate the innate immune system with the conception that an innate immune defect underlies the development of the disease, have been demonstrated a clinical benefit and reinforce this evolving understanding of the disease.
authors.affiliation: Gastrointestinal Unit, Massachusetts General Hospital, 55 Fruit Street, Boston, Massachusetts 02114, USA. kazuofurusho@hotmail.com
authors.forename: Jesus-K
authors.initials: JK
authors.lastname: Yamamoto-Furusho
authors.forename: Joshua-R
authors.initials: JR
authors.lastname: Korzenik
mesh_terms: D003424:Crohn Disease / Q000276:immunology* / Q000503:physiopathology; D004777:Environment; D016178:Granulocyte-Macrophage Colony-Stimulating Factor / Q000235:genetics / Q000502:physiology; D006801:Humans; D007113:Immunity, Innate / Q000235:genetics* / Q000502:physiology; D007413:Intestinal Mucosa / Q000276:immunology / Q000503:physiopathology; D053473:Nod2 Signaling Adaptor Protein / Q000235:genetics / Q000502:physiology; D013601:T-Lymphocytes / Q000502:physiology; D051193:Toll-Like Receptors / Q000235:genetics / Q000502:physiology
chemical_list: C429018:NOD2 protein, human; D053473:Nod2 Signaling Adaptor Protein; D051193:Toll-Like Receptors; D016178:Granulocyte-Macrophage Colony-Stimulating Factor