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Scott D. Boyd

Researcher at Stanford University

Publications -  167
Citations -  13015

Scott D. Boyd is an academic researcher from Stanford University. The author has contributed to research in topics: Antibody & Medicine. The author has an hindex of 42, co-authored 129 publications receiving 9050 citations. Previous affiliations of Scott D. Boyd include Boston Children's Hospital & Massachusetts Institute of Technology.

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Co-evolution of a broadly neutralizing HIV-1 antibody and founder virus

TL;DR: The isolation, evolution and structure of a broadly neutralizing antibody from an African donor followed from the time of infection and its co-crystal structure revealed a new loop-based mechanism of CD4-binding-site recognition.
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Identifying specificity groups in the T cell receptor repertoire

TL;DR: The GLIPH algorithm can analyse large numbers of TCR sequences and define TCR specificity groups shared by TCRs and individuals, which should greatly accelerate the analysis of T cell responses and expedite the identification of specific ligands.
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Determinants of nucleosome organization in primary human cells

TL;DR: This work uses deep sequencing to map nucleosome positions in three primary human cell types and in vitro and unveils an interplay of sequence-based nucleosomal preferences and non-nucleosomal factors in determining nucleosomes organization within mammalian cells.
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Diversity and clonal selection in the human T-cell repertoire.

TL;DR: The results suggest that a highly diverse repertoire is maintained despite thymic involution; however, peripheral fitness selection of T cells leads to repertoire perturbations that can influence the immune response in the elderly.
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B7-1 and B7-2 Have Overlapping, Critical Roles in Immunoglobulin Class Switching and Germinal Center Formation

TL;DR: The results demonstrate that B7-mediated signaling plays a critical role in germinal center formation and immunoglobulin class switching in vivo and that the induction of B 7-1 by adjuvant in B8-2-deficient mice can compensate for the absence of B7,2.