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Sandra O. Gollnick

Researcher at Roswell Park Cancer Institute

Publications -  71
Citations -  12610

Sandra O. Gollnick is an academic researcher from Roswell Park Cancer Institute. The author has contributed to research in topics: Immune system & Major histocompatibility complex. The author has an hindex of 29, co-authored 68 publications receiving 10850 citations. Previous affiliations of Sandra O. Gollnick include Iowa State University.

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Journal Article

Altered Expression of Interleukin 6 and Interleukin 10 As a Result of Photodynamic Therapy in Vivo

TL;DR: It is demonstrated in a BALB/c mouse model that PDT delivered to normal and tumor tissue in vivo causes marked changes in the expression of cytokines interleukin (IL)-6 and IL-10 but not tumor necrosis factor alpha, and suggested that the general inflammatory response to PDT may be mediated at least in part by IL-6.
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p16(Ink4a) and senescence-associated β-galactosidase can be induced in macrophages as part of a reversible response to physiological stimuli.

TL;DR: It is reported that expression of p 16Ink4a and SAβG in macrophages is acquired as part of a physiological response to immune stimuli rather than through senescence, consistent with reports that p16InK4a plays a role in Macrophage polarization and response.
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Photodynamic therapy enhancement of antitumor immunity is regulated by neutrophils

TL;DR: It is shown that a PDT regimen that induced a high level of neutrophilic infiltrate generated tumor-specific primary and memory CD8(+) T-cell responses and may suggest a mechanism by which neutrophils might affect antitumor immunity following other inflammation-inducing cancer therapies.
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IL-6 trans-signaling licenses mouse and human tumor microvascular gateways for trafficking of cytotoxic T cells.

TL;DR: It is reported that homeostatic trafficking of tumor-reactive CD8+ T cells across microvascular checkpoints is limited in tumors despite the presence of inflammatory cytokines, and a causal link was established between IL-6-dependent licensing of tumor vessels for Tem trafficking and apoptosis of tumor targets.
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Peroxiredoxin 1 Stimulates Secretion of Proinflammatory Cytokines by Binding to TLR4

TL;DR: It is demonstrated that incubation of Prx1 with thioglycollate-elicited murine macrophages or immature bone marrow-derived dendritic cells resulted in TLR4-dependent secretion of TNF-α and IL-6 and dendrite cell maturation, suggesting that Prx 1 may act as danger signal similar to other TLR 4-binding chaperone molecules such as HSP72.