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Lori R. Covey

Researcher at Rutgers University

Publications -  48
Citations -  6826

Lori R. Covey is an academic researcher from Rutgers University. The author has contributed to research in topics: CD40 & T cell. The author has an hindex of 23, co-authored 44 publications receiving 6328 citations. Previous affiliations of Lori R. Covey include Howard Hughes Medical Institute & Columbia University.

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Journal ArticleDOI

Guidelines for the use and interpretation of assays for monitoring autophagy (3rd edition)

Daniel J. Klionsky, +2522 more
- 21 Jan 2016 - 
TL;DR: In this paper, the authors present a set of guidelines for the selection and interpretation of methods for use by investigators who aim to examine macro-autophagy and related processes, as well as for reviewers who need to provide realistic and reasonable critiques of papers that are focused on these processes.
Journal Article

CD40 molecules induce down-modulation and endocytosis of T cell surface T cell-B cell activating molecule/CD40-L. Potential role in regulating helper effector function.

TL;DR: It is suggested that CD40 induced T-BAM/CD40-L down-modulation occurs, in part, by receptor-mediated endocytosis followed by lysosomal degradation and may represent a mechanism to regulate CD4+ T cell helper effector functions.
Journal Article

T lymphocyte T cell-B cell-activating molecule/CD40-L molecules induce normal B cells or chronic lymphocytic leukemia B cells to express CD80 (B7/BB-1) and enhance their costimulatory activity.

TL;DR: This report demonstrates that T-BAM/CD40-L molecules on a Jurkat T cell leukemia subclone or nonlymphoid 293 kidney cell transfectants induce B cells or B-CLL cells to express CD80 (B7/BB-1) in a manner that is specifically inhibited by anti-T-Bam/CD 40-L mAb 5C8.
Journal Article

T-BAM/CD40-L on helper T lymphocytes augments lymphokine-induced B cell Ig isotype switch recombination and rescues B cells from programmed cell death.

TL;DR: Data support the idea that T-BAM/CD40-L plays important roles in inducing Ig isotype switch recombination and the clonal selection of isotype-switched B cells.
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Isolation of scid pre-B cells that rearrange kappa light chain genes: formation of normal signal and abnormal coding joins.

TL;DR: The finding that the scid defect prevents formation of correct coding but not signal joins distinguishes these events mechanistically.