Graft-versus-host disease in the absence of the spleen after allogeneic bone marrow transplantation.

BACKGROUND The spleen is considered to be an important secondary lymphoid organ where acute graft-versus-host disease (GVHD) is initiated by donor T cells that recognize host alloantigens after allogeneic bone-marrow transplantation (BMT). The influence of splenectomy on the development of GVHD prior to BMT has yet to be determined. METHODS The mortality and severity of murine GVHD of unsplenectomized, splenectomized, and sham-operated recipients of allogeneic BMT were compared in a blinded fashion. Serum levels of interferon (IFN)-gamma were measured 7 days after BMT, as an index of systemic donor T-cell responses. RESULTS Mortality and morbidity of acute GVHD were not significantly affected by splenectomy in a major histocompatibility complex (MHC)-mismatched, CD4-driven murine GVHD model and a minor histocompatibility antigen (MiHA)-mismatched, CD8-driven GVHD model. Serum levels of IFN-gamma also were not different between the groups. CONCLUSION GVHD can readily develop after allogeneic BMT, even in the absence of the spleen, in these mouse models.

[1]  T. Kakiuchi,et al.  Mice Lacking Expression of the Chemokines Ccl21-Ser and Ccl19 (plt Mice) Demonstrate Delayed but Enhanced T Cell Immune Responses , 2001, The Journal of experimental medicine.

[2]  J. Kirby,et al.  TGF-beta expression in renal transplant biopsies: a comparative study between cyclosporin-A and tacrolimus. , 2000, Transplantation.

[3]  E. Wolf,et al.  CCR7 Coordinates the Primary Immune Response by Establishing Functional Microenvironments in Secondary Lymphoid Organs , 1999, Cell.

[4]  M. V. D. van den Brink,et al.  IL-11 separates graft-versus-leukemia effects from graft-versus-host disease after bone marrow transplantation. , 1999, The Journal of clinical investigation.

[5]  M. Shlomchik,et al.  Prevention of graft versus host disease by inactivation of host antigen-presenting cells. , 1999, Science.

[6]  L. Marinucci,et al.  TGFbeta and TGFalpha, antagonistic effect in vitro on extracellular matrix accumulation by chick skin fibroblasts at two distinct embryonic stages. , 1999, The International journal of developmental biology.

[7]  M. Lagman,et al.  Cyclosporine induces cancer progression by a cell-autonomous mechanism , 1999, Nature.

[8]  G. Nabel.  A transformed view of cyclosporine , 1999, Nature.

[9]  A. Sheil.  Cancer in immune-suppressed organ transplant recipients: aetiology and evolution. , 1998, Transplantation proceedings.

[10]  J. Tollemar,et al.  Urinary tract infections following renal transplantation. , 1998, Transplantation proceedings.

[11]  C. Irwin,et al.  Comparative effects of cyclosporin on glycosaminoglycan synthesis by gingival fibroblasts. , 1997, Journal of periodontology.

[12]  J. Crawford,et al.  An experimental model of idiopathic pneumonia syndrome after bone marrow transplantation: I. The roles of minor H antigens and endotoxin. , 1996, Blood.

[13]  F. Carinci,et al.  Ultrastructural and histochemical features of the ground substance in cyclosporin A-induced gingival overgrowth. , 1996, Journal of periodontology.

[14]  P. Ljungman,et al.  Risk factors for acute graft-versus-host disease in 291 consecutive HLA-identical bone marrow transplant recipients. , 1995, Bone marrow transplantation.

[15]  K. Sullivan,et al.  A retrospective analysis of the long-term effect of splenectomy on late infections, graft-versus-host disease, relapse, and survival after allogeneic marrow transplantation for chronic myelogenous leukemia. , 1995, Blood.

[16]  F. Thaiss,et al.  CYCLOSPORINE STIMULATES EXPRESSION OF TRANSFORMING GROWTH FACTOR-β IN RENAL CELLS POSSIBLE MECHANISM OF CYCLOSPORINES ANTIPROLIFERATIVE EFFECTS , 1995, Transplantation.

[17]  J. Reiffers,et al.  Role of splenectomy in incidence and severity of acute graft-versus-host disease: a multicenter study of 157 patients. , 1991, Bone marrow transplantation.

[18]  T. Laurent,et al.  The properties and turnover of hyaluronan. , 1986, Ciba Foundation symposium.

[19]  B. Nilsson,et al.  DEATH BY GRAFT‐VERSUS‐HOST DISEASE ASSOCIATED WITH HLA MISMATCH, HIGH RECIPIENT AGE, LOW MARROW CELL DOSE, AND SPLENECTOMY , 1985, Transplantation.

[20]  B. Hall.  ROLE OF THE SPLEEN IN CELL‐MEDIATED CARDIAC ALLOGRAFT REJECTION , 1982, Transplantation.

[21]  J. Sprent,et al.  Negative selection of T cells causing lethal graft-versus-host disease across minor histocompatibility barriers. Role of the H-2 complex , 1980, The Journal of experimental medicine.

[22]  M K Patterson,et al.  Measurement of growth and viability of cells in culture. , 1979, Methods in enzymology.