Serum Tumor Necrosis Factor Alpha Associated With Acute Graft-Versus-Host Disease in Humans

Graft-versus-host-disease-associated lymphoid hypoplasia and B cell dysfunction is dependent upon donor T cell-mediated Fas-ligand function, but not perforin function

“…In addition, Wall and Sheehan (13) found that neutralizing anti-TNF-␣ mAb reversed the ability of splenocytes from animals with GVHD to suppress proliferative responses of normal splenocytes to mitogens in vitro. It has also been shown that serum levels of IFN-␥ and TNF-␣ cytokines are elevated in patients following clinical allogeneic BMT (20)(21)(22). In light of such results and based on the present findings, we propose a model in which dysregulation and overproduction of these cytokines contributes to up-regulation of Fas expression on lymphocyte progenitor populations in the marrow post-BMT, resulting in the enhancement of their susceptibility to Fas-induced apoptosis.…”

Anti-tumor necrosis factor-a for the treatment of steroid-refractory acute graft-versus-host disease

“…Tumor necrosis factor alpha (TNF-α) is an important cytokine involved in the pathophysiology of acute GVHD (2)(3)(4)(5). Infliximab is a chimeric human anti-TNF-α IgG1 monoclonal antibody (6).…”

Infliximab use in patients with severe graft-versus-host disease and other emerging risk factors of non-Candida invasive fungal infections in allogeneic hematopoietic stem cell transplant recipients: a cohort study

“…3,4 Patients with grades III to IV GVHD are usually treated with intensification of their immunosuppressive regimen, typically with high-dose corticosteroids; however, there is no standard therapy for patients with GVHD who fail an initial course of corticosteroids. 2 Tumor necrosis factor ␣ (TNF-␣) is an important cytokine involved in the development of GVHD, [5][6][7][8] and studies have shown possible benefit of anti-TNF-␣ antibody administration in treating GVHD. 9,10 Infliximab was administered to patients in our institution for treatment of severe or refractory grades III to IV GVHD, and although responses were observed, many died of opportunistic infections.…”