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Herbert C. Morse

Researcher at National Institutes of Health

Publications -  400
Citations -  23200

Herbert C. Morse is an academic researcher from National Institutes of Health. The author has contributed to research in topics: B cell & Lymphoma. The author has an hindex of 77, co-authored 400 publications receiving 21998 citations. Previous affiliations of Herbert C. Morse include University of Southampton & Istituto Superiore di Sanità.

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A Critical Role for IL-21 in Regulating Immunoglobulin Production

TL;DR: It is demonstrated that, although mice deficient in the receptor for IL-21 (IL-21R) have normal lymphoid development, after immunization, these animals have higher production of the immunoglobulin IgE, but lower IgG1, than wild-type animals, suggesting that these γc-dependent cytokines may be those whose inactivation is primarily responsible for the B cell defect in humans with XSCID.
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TRIM family proteins and their emerging roles in innate immunity

TL;DR: Recent data are described that reveal broader antiviral and antimicrobial activities of TRIM proteins and their involvement in the regulation of pathogen-recognition and transcriptional pathways in host defence is discussed.
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Regulation of B cell differentiation and plasma cell generation by IL-21, a novel inducer of Blimp-1 and Bcl-6

TL;DR: It is demonstrated that although IL-21 induces death of resting B cells, it promotes differentiation of B cells into postswitch and plasma cells, explaining howIL-21 can be proapoptotic for B cells in vitro yet critical for Ag-specific Ig production in vivo.
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ICSBP Is Essential for the Development of Mouse Type I Interferon-producing Cells and for the Generation and Activation of CD8α+ Dendritic Cells

TL;DR: ICSBP is a crucial factor in the regulation of two possibly linked processes: (a) the development and activity of mIPCs, whose lack in ICSBP−/− mice may explain their high susceptibility to virus infections; (b) the generation and activation of CD8α+ DCs, whose impairment in ICD mice can be responsible for the defective generation of a Th1 type of immune response.