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Natasa Strbo

Researcher at University of Miami

Publications -  83
Citations -  2136

Natasa Strbo is an academic researcher from University of Miami. The author has contributed to research in topics: Immune system & Perforin. The author has an hindex of 26, co-authored 74 publications receiving 1783 citations. Previous affiliations of Natasa Strbo include University of Rijeka.

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Innate and Adaptive Immune Responses in Wound Epithelialization

TL;DR: A better understanding of the epithelial cells (keratinocytes), immune cells, and mechanisms that contribute to an effective wound healing process is necessary so that new strategies for successful wounds treatment can be devised.
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Age-Related Decline of Perforin Expression in Human Cytotoxic T Lymphocytes and Natural Killer Cells

TL;DR: Functional tests clearly showed the deficiency in early spontaneous cytotoxic potential of PBL from elderly persons due to relative P deficiency, which can be corrected by stimulation of cytolytic cells with target cells and interleukin-2 (IL-2).
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Identification of a subpopulation of macrophages in mammary tumor-bearing mice that are neither M1 nor M2 and are less differentiated.

TL;DR: The results suggest that T-PEMs are less differentiated and represent a newly derived population from blood monocytes, and show that transforming growth factor-beta and prostaglandin E(2), two immunosuppressive tumor-derived factors, may be involved in this phenomenon.
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Differential effects of IL-21 and IL-15 on perforin expression, lysosomal degranulation, and proliferation in CD8 T cells of patients with human immunodeficiency virus-1 (HIV).

TL;DR: CD8 T cells of patients with HIV can be modulated by IL-21 to increase perforin expression without undergoing overt cellular activation, and could potentially be useful for its per forin-enhancing properties in anti-HIV immunotherapy.
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Deregulated immune cell recruitment orchestrated by FOXM1 impairs human diabetic wound healing.

TL;DR: The role of a perturbed, ineffective inflammatory response is underscored as a major contributor to the pathogenesis of DFUs, which is facilitated by FOXM1-mediated deregulation of recruitment of neutrophils and macrophages, revealing a potential therapeutic strategy.