Publications by authors named "G K Babcock"

Article Synopsis
  • Long-term organ transplant survival is hindered by life-long immunosuppression, which increases risks of infections and other complications.
  • Expanding regulatory T cells (Tregs) using a newly designed IL-2 variant (mIL-2) can help reduce immunosuppression and improve graft outcomes.
  • In experiments, mIL-2 successfully expanded Tregs in mouse models and primates, promoting donor-specific tolerance and enhancing immune regulation for better allograft survival.
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The increase in emerging drug resistant Gram-negative bacterial infections is a global concern. In addition, there is growing recognition that compromising the microbiota through the use of broad-spectrum antibiotics can impact long term patient outcomes. Therefore, there is the need to develop new bactericidal strategies to combat Gram-negative infections that would address these specific issues.

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SARS coronavirus 1 (SARS-CoV-1) causes a respiratory infection that can lead to acute respiratory distress characterized by inflammation and high levels of cytokines in the lung tissue. In this study we constructed a herpes simplex virus 1 replication-defective mutant vector expressing SARS-CoV-1 spike protein as a potential vaccine vector and to probe the effects of spike protein on host cells. The spike protein expressed from this vector is functional in that it localizes to the surface of infected cells and induces fusion of ACE2-expressing cells.

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Introduction: Negative Pressure Wound Therapy (NPWT) is a procedure used for nonhealing wounds. In NPWT, a special sealed dressing of large cell foam (>400 µm) or gauze is connected to a pump. Most commonly, negative pressures between -10 and -125 millimeters of mercury (mm Hg) are used.

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Therapeutically targeting CD138, a define multiple myeloma (MM) antigen, is not yet approved for patients. We here developed and determined the preclinical efficacy of VIS832, a novel therapeutic monoclonal antibody (MoAb) with differentiated CD138 target binding to BB4 that is anti-CD138 MoAb scaffold for indatuximab ravtansine (BT062). VIS832 demonstrated enhanced CD138-binding avidity and significantly improved potency to kill MM cell lines and autologous patient MM cells regardless of resistance to current standard-of-care therapies, via robust antibody-dependent cellular cytotoxicity and phagocytosis mediated by NK and macrophage effector cells, respectively.

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