title: The pathophysiology and treatment of graft-versus-host disease.
abstract: Acute and chronic GVHD remain major impediments to the wider application of allogeneic marrow transplantation. It is presumed that human acute GVHD is analogous to the murine model which is initiated by donor T lymphocytes reacting with recipient 'minor' histocompatibility antigens. Chronic GVHD may result from immunoaggression of donor lymphoid cells that have developed and differentiated within the host. Lack of GVHD (i.e., the development of tolerance) may be due either to generation within the host of specific suppressor lymphocytes or to clonal deletion of alloreactive donor cells. Over the last five years progress has been made in the recognition, early diagnosis and successful therapy of chronic GVHD. Methods of prevention and therapy of acute GVHD are still largely unsuccessful. With improved understanding of immune regulation, it is hoped that GVHD can be eliminated in patients transplanted for non-malignant conditions and adroitly modified (without loss of anti-leukaemic potential) in patients with malignant disorders. The challenge of the coming decade is to reach these goals while speeding the return of full immunological competence in the marrow transplant recipient.
mesh_terms: D000208:Acute Disease; D000818:Animals; D016026:Bone Marrow Transplantation; D002908:Chronic Disease; D003524:Cyclosporins / Q000008:administration & dosage; D003586:Cytomegalovirus Infections / Q000209:etiology / Q000276:immunology; D006086:Graft vs Host Disease / Q000276:immunology / Q000473:pathology / Q000503:physiopathology*; D006561:Herpes Simplex / Q000209:etiology / Q000276:immunology; D006648:Histocompatibility; D006801:Humans; D007108:Immune Tolerance; D007938:Leukemia / Q000628:therapy; D008727:Methotrexate / Q000008:administration & dosage; D051379:Mice; D011379:Prognosis; D013601:T-Lymphocytes / Q000276:immunology
chemical_list: D003524:Cyclosporins; D008727:Methotrexate