Graft-versus-Host Disease in Bone Marrow Transplantation: Experimental, Laboratory, and Clinical Contributions of the Last Few Years

Abstract

Graft-versus-host disease (GVHD) is a major and often lethal complication of bone marrow transplantation. Research of the past few years has greatly expanded our understanding of the disease and enriched the arsenal of preventive and therapeutic procedures. The present review attempts to give a survey of experimental and clinical GVHD, updating essential knowledge with the latest information until July 1993. The covered topics include the complex immune pathomechanism of acute and chronic GVHD in murine models, the pathogenic role of major, minor, and other antigenic disparities, laboratory markers predicting GVHD, factors influencing appearance and course of the disease, the relationship between GVHD and the graft-versus-leukemia effect, and novel experimental and clinically tested preventive and therapeutic modalities. Finally, the authors set forth their perspective on the most relevant questions in GVHD-related research.

Idiopathic pneumonia syndrome after bone marrow transplantation: the role of pre-transplant radiation conditioning and local cytokine dysregulation in promoting lung inflammation and fibrosis

“…Although it is unclear which cells mediate GVHD and IPS, or what the exact specificity of the reactive cell is, it is reasonable to hypothesize at this juncture that chronic activation of macrophages and T cells, and subsequent cytokine release in the interstitial space, is responsible for tissue remodelling after injury ± a consequence that results in fibrosis in the lungs. Given the importance of both CD4 1 and CD8 1 T cells in GVHD (Jadus & Wepsic 1992;Kelemen et al 1993) importance of T cells in a variety of chronic lung injury models, it is highly conceivable that T cells contribute to the onset and progression of IPS, directly through effector cell functions and indirectly through cytokine release and cytokine-mediated effects on other cells. The importance of progressive development of CD4 1 T cell inflammation in the development of fibrosis may be two-fold.…”

Treatment of mice with anti-CD44 after allogeneic bone marrow cell transplantation is lethal

“…For these reasons, besides others, bone marrow cell (BMC) transplantation has become an important field of interest [1][2][3]. One of the questions being presently explored refers to the advantage of the anti-tumor reactivity observed after allogeneic BMC transplantation without meeting the disadvantage of graft-versus-host (GVH) disease or graft rejection [4][5][6]. We were interested in whether CD44 could be of functional relevance in the acceptance of allogeneic bone marrow grafts and whether anti-CD44 would influence GVH and host versus graft (HVG) reactivities.…”

Prevention and treatment of acute graft-versus-host disease: the old and the new. A report from The Eastern Cooperative Oncology Group (ECOG)

“…37 A variety of techniques have been used to deplete lymphocytes from the donor graft, including monoclonal anti-Despite a number of significant complications such as avascular necrosis of bone (relative risk 6.3, P = 0.0002), body, chemical, and physical separation methods. [176][177][178][179][180][181][182][183][184][185][186][187][188][189][190][191][192][193][194] An overview is extremely difficult, since there is no standard corticosteroids form the backbone of most regimens for treatment of acute GVHD. 15,218,219 Weisdorf and co-work-approach.…”