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Sladjana Skopelja-Gardner, Lucrezia Colonna, Payton Hermanson, Xizhang Sun, Lena Tanaka, Joyce Tai, Yenly Nguyen, Jessica M. Snyder, Charles E. Alpers, Kelly L. Hudkins, David J. Salant, YuFeng Peng and Keith B. Elkon J Immunol May 15, 2020, 204 (10) 2627-2640; DOI: https://doi.org/10.4049/jimmunol.1901473 Key Points Novel TM lupus mouse strains develop spontaneous nephritis. In C1q deficiency, kidney complement activation likely occurred via the LP.
Sladjana Skopelja-Gardner, Lucrezia Colonna, Payton Hermanson, Xizhang Sun, Lena Tanaka, Joyce Tai, Yenly Nguyen, Jessica M. Snyder, Charles E. Alpers, Kelly L. Hudkins, David J. Salant, YuFeng Peng and Keith B. Elkon J Immunol April 1, 2020, ji1901473; DOI: https://doi.org/10.4049/jimmunol.1901473 Key Points Novel TM lupus mouse strains develop spontaneous nephritis. In C1q deficiency, kidney complement activation likely occurred via the LP.
Three key factors are widely believed to have contributed to the cure of the Berlin patient: (1) the conditioning regimen used for his two transplants, (2) the use of donor cells containing a homozygous HIV-resistant CCR5Δ32 mutation42, and (3) the development of post-transplant GVHD43, which is hypothesized to help clear the HIV reservoir through an as-yet ill-defined GVVR effect. The Boston Patients14, underwent allogeneic HCT and developed GVHD, but received HIV-susceptible donor cells.
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