Methods of handling, thawing, and infusion of cord blood (CB) products vary substantially among thaw/transplant centers (TCs). This review 1) compares currently available CB product types and thaw methods recommended by CB banks (CBBs), 2) discusses causes of inconsistency in thaw method application at TCs, 3) advises elements to consider in thaw method approval or selection at the TC, 4) provides a procedural template for the traditional thaw methods, and 5) suggests acceptable time from product thaw to infusion and other considerations for safe infusion. It also compares postinfusion adverse reaction and engraftment data as functions of thaw methods. Remarks and suggestions made throughout this review are: 1) not intended to supersede manufacturer's instructions but meant to support the standardization of preparative procedures recommended by CBBs and 2) intended to help TCs to investigate relevant quality issues and handle challenges, especially when the TC is unable to follow recommendations due to foreseeable technical, quality, and/or clinical factors.
The retrovirus human T cell leukemia virus (HTLV) type I (HTLV-I) is primarily transmitted by breast-feeding or sexual contact, by cell-to-cell contact between T cells. TGF-β, which has been shown to enhance transmission of HTLV-I in vitro, is found at high levels in breast milk and semen. In this study, the ability of TGF-β to regulate expression of molecules involved in HTLV-I binding and entry was examined. Previous studies using a soluble form of the HTLV-I envelope protein SU have shown that quiescent human T cells do not express cell surface molecules that specifically bind SU. After T cell activation, HTLV SU binding proteins are rapidly induced. In this study, we report that TGF-β induces expression of proteins that bind soluble HTLV SU and HTLV virions on naive CD4+ T lymphocytes. The induction of these proteins occurred without cell cycle entry or expression of activation markers, involved TGF-β-induced intracellular signaling, and required de novo transcription and translation. Treatment of naive CD4+ T lymphocytes with TGF-β induced expression of GLUT-1, which has recently been reported to function as a receptor for HTLV. Treatment of a TGF-β-sensitive human myeloid cell line increased the titer of both HTLV-I- and HTLV-II-pseudotyped viruses. Although earlier studies suggested that HTLV SU binding proteins might be an early marker of T cell activation and/or cell proliferation, we report in this study that TGF-β induces binding of HTLV virions and expression of glucose transporter type 1 in primary CD4+ T lymphocytes that remain quiescent.
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