scispace - formally typeset
J

Jesse C. Nussbaum

Researcher at University of California, San Francisco

Publications -  21
Citations -  4538

Jesse C. Nussbaum is an academic researcher from University of California, San Francisco. The author has contributed to research in topics: Innate lymphoid cell & Inflammation. The author has an hindex of 16, co-authored 20 publications receiving 3767 citations. Previous affiliations of Jesse C. Nussbaum include University of North Carolina at Chapel Hill & Merck & Co..

Papers
More filters
Journal ArticleDOI

Type 2 innate lymphoid cells control eosinophil homeostasis

TL;DR: It is shown that serum IL-5 levels are maintained by long-lived type 2 innate lymphoid cells (ILC2) resident in peripheral tissues, and this dissociated regulation can be tuned by nutrient intake and central circadian rhythms.
Journal ArticleDOI

Innate lymphoid type 2 cells sustain visceral adipose tissue eosinophils and alternatively activated macrophages

TL;DR: Innate lymphoid type 2 cells maintain eosinophils and alternatively activated macrophages in visceral fat via the production of IL-5 and IL-13.
Journal ArticleDOI

Activated type 2 innate lymphoid cells regulate beige fat biogenesis

TL;DR: It is reported here that activation of ILC2s by IL-33 is sufficient to promote the growth of functional beige fat in thermoneutral mice and highlights a critical role for I LC2s and type 2 cytokines in the regulation of adipocyte precursor numbers and fate, and as a consequence, adipose tissue homeostasis.
Journal ArticleDOI

InterleuKin-33 And Interferon-Γ Counter-Regulate Group 2 Innate Lymphoid Cell Activation During Immune Perturbation

TL;DR: Interleukin-33 mediates activation of ILC2s and Treg cells in resting adipose tissue, but also after helminth infection or treatment with IL-2, and IFN-γ suppresses this pathway, likely to promote inflammatory responses and divert metabolic resources necessary to protect the host.
Journal ArticleDOI

Tissue signals imprint ILC2 identity with anticipatory function.

TL;DR: Tissue-specific imprinting dictates the activating receptors ILC2s express, even in germ-free mice, and it is shown that endogenous, tissue-derived signals drive the maturation of I LC2 subsets by controlling expression of distinct patterns of activating receptors, thus anticipating tissue-specific perturbations occurring later in life.