7 results match your criteria: "Harvard Medical School and Mass General Brigham[Affiliation]"

Transcription factor TCF1 binds to RORγt and orchestrates a regulatory network that determines homeostatic Th17 cell state.

Immunity

November 2024

Gene Lay Institute of Immunology and Inflammation, Ann Romney Center for Neurologic Diseases, Harvard Medical School and Mass General Brigham, Boston, MA 02115, USA; Broad Institute of MIT and Harvard, Cambridge, MA 02142, USA. Electronic address:

T helper (Th) 17 cells encompass a spectrum of cell states, including cells that maintain homeostatic tissue functions and pro-inflammatory cells that can drive autoimmune tissue damage. Identifying regulators that determine Th17 cell states can identify ways to control tissue inflammation and restore homeostasis. Here, we found that interleukin (IL)-23, a cytokine critical for inducing pro-inflammatory Th17 cells, decreased transcription factor T cell factor 1 (TCF1) expression.

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Purpose Of Review: Atypical chemokine receptor-1 (ACKR1)/Duffy antigen receptor of chemokines (DARC)-associated neutropenia (ADAN; OMIM 611862), previously named benign ethnic neutropenia, and present in two-thirds of individuals identifying as Black in the USA, is associated with mild to moderate decreases in peripheral neutrophil counts that nevertheless do not lead to increased infections. Consequently, recent initiatives have sought to establish normal neutrophil count reference ranges for ADAN, considering it a normal variant rather than a clinical disorder requiring medical intervention.

Recent Findings: A limited number of studies elucidating the mechanism of neutropenia in ADAN has suggested that neutrophils may redistribute from peripheral blood to the tissues including the spleen: this might explain why ADAN is not associated with increased risks of infection since the total number of neutrophils in the body remains normal.

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A Single-Atom Manganese Nanozyme Mn-N/C Promotes Anti-Tumor Immune Response via Eliciting Type I Interferon Signaling.

Adv Sci (Weinh)

April 2024

State Key Laboratory of Systems Medicine for Cancer, Renji-Med X Clinical Stem Cell Research Center, Ren Ji Hospital, School of Medicine, Shanghai Jiao Tong University, Shanghai, 200127, China.

Tumor microenvironment (TME)-induced nanocatalytic therapy is a promising strategy for cancer treatment, but the low catalytic efficiency limits its therapeutic efficacy. Single-atom catalysts (SACs) are a new type of nanozyme with incredible catalytic efficiency. Here, a single-atom manganese (Mn)-N/C nanozyme is constructed.

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Opportunistic Screening: Scientific Expert Panel.

Radiology

June 2023

From the Departments of Radiology (P.J.P., J.W.G.) and Medical Physics (J.W.G.), University of Wisconsin School of Medicine & Public Health, E3/311 Clinical Science Center, 600 Highland Ave, Madison, WI 53792-3252; Imaging Biomarkers and Computer-Aided Diagnosis Laboratory, Radiology and Imaging Sciences, National Institutes of Health Clinical Center, Bethesda, Md (R.M.S.); Department of Radiology and Medical Imaging, University of Virginia School of Medicine, Charlottesville, Va (A.K.); Lenox Hill Radiology, New York, NY (S.A.); Harvard Medical School and Mass General Brigham, Boston, Mass (K.J.D.); and Hackensack Radiology Group, Hackensack, NJ (G.N.N.).

Radiologic tests often contain rich imaging data not relevant to the clinical indication. Opportunistic screening refers to the practice of systematically leveraging these incidental imaging findings. Although opportunistic screening can apply to imaging modalities such as conventional radiography, US, and MRI, most attention to date has focused on body CT by using artificial intelligence (AI)-assisted methods.

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Learning from the nexus of autoimmunity and cancer.

Immunity

February 2023

Evergrande Center for Immunologic Diseases, Ann Romney Center for Neurologic Diseases, Harvard Medical School and Mass General Brigham, Boston, MA 02115, USA. Electronic address:

The immune system plays critical roles in both autoimmunity and cancer, diseases at opposite ends of the immune spectrum. Autoimmunity arises from loss of T cell tolerance against self, while in cancer, poor immunity against transformed self fails to control tumor growth. Blockade of pathways that preserve self-tolerance is being leveraged to unleash immunity against many tumors; however, widespread success is hindered by the autoimmune-like toxicities that arise in treated patients.

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Steroid hormone regulation of immune responses in cancer.

Immunometabolism (Cobham)

October 2022

Pelotonia Institute for Immuno-Oncology, OSUCCC-James, The Ohio State University, Columbus, OH, USA.

Steroid hormones are derived from cholesterol and can be classified into sex hormones (estrogens, androgens, progesterone) that are primarily synthesized in the gonads and adrenal hormones (glucocorticoids and mineralocorticoids) that are primarily synthesized in the adrenal gland. Although, it has long been known that steroid hormones have potent effects on the immune system, recent studies have led to renewed interest in their role in regulating anti-tumor immunity. Extra-glandular cells, such as epithelial cells and immune cells, have been shown to synthesize glucocorticoids and thereby modulate immune responses in the tumor microenvironment.

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