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Terry B. Strom

Researcher at Beth Israel Deaconess Medical Center

Publications -  373
Citations -  27700

Terry B. Strom is an academic researcher from Beth Israel Deaconess Medical Center. The author has contributed to research in topics: Transplantation & T cell. The author has an hindex of 82, co-authored 373 publications receiving 26714 citations. Previous affiliations of Terry B. Strom include University of Cologne.

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Phe496 and Leu497 are essential for receptor binding and cytotoxic action of the murine interleukin-4 receptor targeted fusion toxin DAB389-mIL-4.

TL;DR: It is demonstrated that deletion of the C-terminal 15 amino acids of the fusion toxin leads to loss of cytotoxicity and the substitution of Phe496 with either Pro, Ala or Tyr results in a greater than 20-fold decrease in cytotoxic activity of the respective mutant fusion toxins.
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Addition of an IL-15 mutant/FCγ2A antagonist protein protects islet allografts from rejection overriding costimulation blockade

TL;DR: It is hypothesized that targeting the IL-15/IL-15R system in conjunction with costimulation blockade would provide a new perspective for inducing allograft tolerance and reduce immune activation and provides a powerful inhibition of alloimmune responses in both rodents and primates.
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Similar effects of cyclosporine and verapamil on lymphokine, interleukin 2 receptor, and proto-oncogene expression.

TL;DR: The results help clarify the mode of CsA action and may provide a new tool to dissect the early events of T cell activation, while an increase of intracellular Ca2+ may provide the additional signal for IL-2 gene expression.
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The early (18-hr) human mixed lymphocyte reaction: identification and isolation of activated T-cell clones.

TL;DR: This study provides direct evidence that de novo expression of the activation antigens B1 49.9 (49.9) (interleukin-2 receptor) and 4F2 enables identification of alloactivated cells within 18 hr of initiation of human mixed lymphocyte reactions (MLR).
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Differential antibody responses to Ag-B (A region) and Ia (B region) antigens during enhancement of rat renal allografts.

TL;DR: Rat renal allograft survival may be enhanced by active preimmunization, or by passive transfer of antidonor antibodies, but antibody responses to gene products of different regions of the rat major histocompatibility complex (MHC) are not identical in states of rejection, passive, or active enhancement.