The most critical period for surveillance of bacteremic patients was in months 2 through 6 after discharge, during which time, the percentage of patients surviving decreased dramatically. The degree of physiologic derangement, as measured by the Acute Physiology Score, was a useful measure of prognosis within the first month after the score was assessed at ICU admission. However, beyond this period, prognostic utility decreased significantly. Healthcare providers should use caution concerning the expected survival of hospitalized patients with human immunodeficiency virus, based on experience with distinct conditions, such as malignancies.
The role of IL-33 particularly in tumor growth and tumor immunity remains ill defined. We show here that exogenous IL-33 can induce robust antitumor effect through a CD8+ T cell-dependent mechanism. Systemic administration of recombinant IL-33 (rIL-33) alone was sufficient to inhibit growth of established tumors in both transplant and de novo melanoma tumorigenesis models. Notably, in addition to a direct action on CD8+ T cell expansion and IFN-γ production, rIL-33 therapy activated myeloid dendritic cells (mDCs) in tumor-bearing mice, restored antitumor T cell activity and increased antigen cross-presentation within the tumor microenvironment. Furthermore, combination therapy with rIL-33 and agonistic anti-CD40 antibodies demonstrated synergistic antitumor activity. Specifically, MyD88, an essential component of the IL-33 signaling pathway, was required for the IL-33-mediated increase in mDC number and upregulation of costimulatory molecule expression. Importantly, we identified that the IL-33 receptor ST2, MyD88 and STAT1 cooperate to induce costimulatory molecule expression on mDCs in response to rIL-33. Our study has thus revealed a novel IL-33-ST2-MyD88-STAT1 axis that restores mDC activation and maturation in established cancer, and thereby the magnitude of anti-tumor immune responses, suggesting a potential use of rIL-33 as a new immunotherapy option to treat established cancer.
scite is a Brooklyn-based organization that helps researchers better discover and understand research articles through Smart Citations–citations that display the context of the citation and describe whether the article provides supporting or contrasting evidence. scite is used by students and researchers from around the world and is funded in part by the National Science Foundation and the National Institute on Drug Abuse of the National Institutes of Health.
customersupport@researchsolutions.com
10624 S. Eastern Ave., Ste. A-614
Henderson, NV 89052, USA
This site is protected by reCAPTCHA and the Google Privacy Policy and Terms of Service apply.
Copyright © 2024 scite LLC. All rights reserved.
Made with 💙 for researchers
Part of the Research Solutions Family.