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Veera Panova

Researcher at Laboratory of Molecular Biology

Publications -  5
Citations -  1056

Veera Panova is an academic researcher from Laboratory of Molecular Biology. The author has contributed to research in topics: Innate lymphoid cell & Inflammation. The author has an hindex of 4, co-authored 4 publications receiving 952 citations. Previous affiliations of Veera Panova include Francis Crick Institute.

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Journal ArticleDOI

IL-33 is more potent than IL-25 in provoking IL-13–producing nuocytes (type 2 innate lymphoid cells) and airway contraction

TL;DR: This paper showed that IL-33 plays a critical role in the rapid induction of airway contraction by stimulating the prompt expansion of IL-13-producing type 2 innate lymphoid cells, whereas IL-25 induced responses are slower and less potent.
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IL-33 citrine reporter mice reveal the temporal and spatial expression of IL-33 during allergic lung inflammation

TL;DR: It is found that type‐2 pneumocytes constitute the major source of IL‐33 upon allergic lung inflammation following exposure to OVA, fungal extract or ragweed pollen and a potential mechanism of action by which IL‐ 33 rapidly initiates type-2 immune responses is demonstrated.
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Group-2 innate lymphoid cell-dependent regulation of tissue neutrophil migration by alternatively activated macrophage-secreted Ear11.

TL;DR: It is demonstrated that type-2 immune-associated neutrophil infiltration is regulated by the mouse RNase A homologue, eosinophil-associated ribonuclease 11 (Ear11), which is secreted by AAM downstream of IL-25-stimulated ILC2, which helps maintain tissue neutrophils at homoeostasis and during type-1 reactions when chemokine-producing classically activated macrophages are infrequently elicited.
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Apoptotic cell fragments locally activate tingible body macrophages in the germinal center

TL;DR: In this paper , a lymph node resident, CD169-lineage, CSF1R-blockade-resistant precursor is prepositioned in the follicle to prevent secondary necrosis and autoimmune activation by intracellular self antigens.