期刊
BLOOD
卷 110, 期 2, 页码 783-786出版社
AMER SOC HEMATOLOGY
DOI: 10.1182/blood-2006-10-054510
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- NCI NIH HHS [P20 CA103694, P20-CA103694, CA107096, P01 CA033049, R01 CA107096, CA33049] Funding Source: Medline
- NHLBI NIH HHS [HL69929, R01 HL069929] Funding Source: Medline
Tumor necrosis factor (TNF) plays an important role in graft-versus-host disease (GVHD) and graft-versus-tumor (GVT) activity after allogeneic bone marrow transplantation (allo-BMT). TNF can be expressed in a membrane-bound form (memTNF) and as a soluble (solTNF) molecule after being cleaved by the TNF-alpha converting enzyme (TACE). To study the contribution of donor T-cell-derived memTNF versus soITNF in GVHD and GVT, we used mice containing a noncleavable allele in place of endogenous TNF (memTNF(Delta/Delta)) as donors in murine BMT models. Recipients of memTNF T cells developed significantly less GVHD than recipients of wild-type (wt) T cells. In contrast, GVT activity mediated by memTNF T cells remained intact, and alloreactive memTNF T cells showed no defects in proliferation, activation, and cytotoxicity. These data suggest that suppressing the secretion of soITNF by donor T cells significantly decreases GVHD without impairing GVT activity.
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