期刊
JOURNAL OF CLINICAL INVESTIGATION
卷 112, 期 1, 页码 101-108出版社
AMER SOC CLINICAL INVESTIGATION INC
DOI: 10.1172/JCI200317601
关键词
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资金
- NHLBI NIH HHS [R01 HL066279, K08 HL03979-02, R01 HL66279] Funding Source: Medline
- NIAID NIH HHS [T32 AI07109-23-25] Funding Source: Medline
Graft-versus-host disease (GVHD) remains a major cause of morbidity and mortality in allogeneic stem cell transplantation (alloSCT). Donor T cells that accompany stem cell grafts cause GVHD by attacking recipient tissues; therefore, all patients receive GVHD prophylaxis by depletion of T cells from the allograft or through immunosuppressant drugs. In addition to providing a graft-versus-leukemia effect, donor T cells are critical for reconstituting T cell-mediated immunity. Ideally, immunity to infectious agents would be transferred from donor to host without GVHD. Most donors have been exposed to common pathogens and have an increased precursor frequency of memory T cells against pathogenic antigens. We therefore asked whether memory CD62L-CD44(+) CD4(+)T cells would induce less GVHD than unfractionated or naive CD4(+) T cells. Strikingly, we found that memory CD4 cells induced neither clinical nor histologic GVHD. This effect was not due to the increased number of CD4(+)CD25(+) regulatory T cells found in the CD62L(-)CD44(+) fraction because memory T cells depletion of these cells did not cause GVHD. Memory CD4 cells engrafted and responded to antigen both in vivo and in vitro. If these murine results are applicable to human alloSCT, selective administration of memory T cells could greatly improve post-transplant immune reconstitution.
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