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Article ; Online: Increasing vaccination rates requires a better understanding of vaccine hesitancy.

Bennett, Joshua P

CMAJ : Canadian Medical Association journal = journal de l'Association medicale canadienne

2019 Volume 191, Issue 42, Page(s) E1167–E1168

MeSH term(s)	Disease Outbreaks ; Humans ; Measles ; Vaccination ; Vaccines
Chemical Substances	Vaccines
Language	English
Publishing date	2019-10-16
Publishing country	Canada
Document type	Letter ; Comment
ZDB-ID	215506-0
ISSN	1488-2329 ; 0008-4409 ; 0820-3946
ISSN (online)	1488-2329
ISSN	0008-4409 ; 0820-3946
DOI	10.1503/cmaj.73258
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Article ; Online: IRAK1 and IRAK4 as emerging therapeutic targets in hematologic malignancies.

Bennett, Joshua / Starczynowski, Daniel T

Current opinion in hematology

2021 Volume 29, Issue 1, Page(s) 8–19

Abstract: Purpose of review: Cell intrinsic and extrinsic perturbations to inflammatory signaling pathways are a hallmark of development and progression of hematologic malignancies. The interleukin 1 receptor-associated kinases (IRAKs) are a family of related ... ...

Abstract	Purpose of review: Cell intrinsic and extrinsic perturbations to inflammatory signaling pathways are a hallmark of development and progression of hematologic malignancies. The interleukin 1 receptor-associated kinases (IRAKs) are a family of related signaling intermediates (IRAK1, IRAK2, IRAK3, IRAK4) that operate at the nexus of multiple inflammatory pathways implicated in the hematologic malignancies. In this review, we explicate the oncogenic role of these kinases and review recent therapeutic advances in the dawning era of IRAK-targeted therapy. Recent findings: Emerging evidence places IRAK signaling at the confluence of adaptive resistance and oncogenesis in the hematologic malignancies and solid tissue tumors. Preclinical investigations nominate the IRAK kinases as targetable molecular dependencies in diverse cancers. Summary: IRAK-targeted therapies that have matriculated to early phase trials are yielding promising preliminary results. However, studies of IRAK kinase signaling continue to defy conventional signaling models and raise questions as to the design of optimal treatment strategies. Efforts to refine IRAK signaling mechanisms in the malignant context will inspire deliberate IRAK-targeted drug development and informed combination therapy.
MeSH term(s)	Hematologic Neoplasms/drug therapy ; Humans ; Interleukin-1 Receptor-Associated Kinases/genetics ; Interleukin-1 Receptor-Associated Kinases/metabolism ; Signal Transduction
Chemical Substances	IRAK1 protein, human (EC 2.7.11.1) ; IRAK4 protein, human (EC 2.7.11.1) ; Interleukin-1 Receptor-Associated Kinases (EC 2.7.11.1)
Language	English
Publishing date	2021-11-08
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	1153887-9
ISSN	1531-7048 ; 1065-6251
ISSN (online)	1531-7048
ISSN	1065-6251
DOI	10.1097/MOH.0000000000000693
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Article ; Online: Rheumatoid sarcopenia: loss of skeletal muscle strength and mass in rheumatoid arthritis.

Bennett, Joshua L / Pratt, Arthur G / Dodds, Richard / Sayer, Avan A / Isaacs, John D

Nature reviews. Rheumatology

2023 Volume 19, Issue 4, Page(s) 239–251

Abstract: Sarcopenia, a disorder that involves the generalized loss of skeletal muscle strength and mass, was formally recognized as a disease by its inclusion in the International Classification of Diseases in 2016. Sarcopenia typically affects older people, but ... ...

Abstract	Sarcopenia, a disorder that involves the generalized loss of skeletal muscle strength and mass, was formally recognized as a disease by its inclusion in the International Classification of Diseases in 2016. Sarcopenia typically affects older people, but younger individuals with chronic disease are also at risk. The risk of sarcopenia is high (with a prevalence of ≥25%) in individuals with rheumatoid arthritis (RA), and this rheumatoid sarcopenia is associated with increased likelihood of falls, fractures and physical disability, in addition to the burden of joint inflammation and damage. Chronic inflammation mediated by cytokines such as TNF, IL-6 and IFNγ contributes to aberrant muscle homeostasis (for instance, by exacerbating muscle protein breakdown), and results from transcriptomic studies have identified dysfunction of muscle stem cells and metabolism in RA. Progressive resistance exercise is an effective therapy for rheumatoid sarcopenia but it can be challenging or unsuitable for some individuals. The unmet need for anti-sarcopenia pharmacotherapies is great, both for people with RA and for otherwise healthy older adults.
MeSH term(s)	Humans ; Aged ; Sarcopenia/etiology ; Sarcopenia/epidemiology ; Sarcopenia/metabolism ; Muscle Strength ; Muscle, Skeletal/pathology ; Arthritis, Rheumatoid/complications ; Arthritis, Rheumatoid/epidemiology ; Arthritis, Rheumatoid/drug therapy ; Inflammation/pathology
Language	English
Publishing date	2023-02-17
Publishing country	United States
Document type	Journal Article ; Review
ZDB-ID	2491532-4
ISSN	1759-4804 ; 1759-4790
ISSN (online)	1759-4804
ISSN	1759-4790
DOI	10.1038/s41584-023-00921-9
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Article ; Online: Closed Collaborative Surgical Intensive Care Unit Modeling and Its Association With Trauma Patient Outcomes.

Yao, Tianyuan / Jensen, Hanna K / Reif, Rebecca J / Kimbrough, Mary K / Schlortt, Kiley R / Bennett, Joshua W / Bhavaraju, Avi

The Journal of surgical research

2022 Volume 283, Page(s) 494–499

Abstract: Introduction: The optimization of intensive care unit (ICU) care impacts clinical outcomes and resource utilization. In 2017, our surgical ICU (SICU) adopted a "closed-collaborative" model. The aim of this study is to compare patient outcomes in the ... ...

Abstract	Introduction: The optimization of intensive care unit (ICU) care impacts clinical outcomes and resource utilization. In 2017, our surgical ICU (SICU) adopted a "closed-collaborative" model. The aim of this study is to compare patient outcomes in the closed-collaborative model versus the previous open model in a cohort of trauma surgical patients admitted to our adult level 1 trauma center. Methods: A retrospective review of trauma patients in the SICU from August 1, 2015 to July 31, 2019 was performed. Patients were divided into those admitted prior to August 1, 2017 (the "open" cohort) and those admitted after August 1, 2017 (the "closed-collaborative" cohort). Demographic variables and clinical outcomes were analyzed. Trauma severity was assessed using injury severity score (ISS). Results: We identified 1669 patients (O: 895; C: 774). While no differences in demographics were observed, the closed-collaborative cohort had a higher overall ISS (O: 21.5 ± 12.14; C: 25.10 ± 2.72; P < 0.0001). There were no significant differences between the two cohorts in the incidence of strokes (O: 1.90%; C: 2.58%, P = 0.3435), pulmonary embolism (O: 0.78%; C: 0.65%; P = 0.7427), sepsis (O: 5.25%; C: 7.49%; P = 0.0599), median ICU charges (O: $7784.50; C: $8986.53; P = 0.5286), mortality (O: 11.40%; C: 13.18%; P = 0.2678), or ICU length of stay (LOS) (O: 4.85 ± 6.23; C: 4.37 ± 4.94; P = 0.0795). Conclusions: Patients in the closed-collaborative cohort had similar clinical outcomes despite having a sicker cohort of patients. We hypothesize that the closed-collaborative ICU model was able to maintain equivalent outcomes due to the dedicated multidisciplinary critical care team caring for these patients. Further research is warranted to determine the optimal model of ICU care for trauma patients.
MeSH term(s)	Adult ; Humans ; Intensive Care Units ; Retrospective Studies ; Trauma Centers ; Length of Stay ; Critical Care
Language	English
Publishing date	2022-11-24
Publishing country	United States
Document type	Journal Article
ZDB-ID	80170-7
ISSN	1095-8673 ; 0022-4804
ISSN (online)	1095-8673
ISSN	0022-4804
DOI	10.1016/j.jss.2022.11.015
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Article ; Online: The Rheumatoid Arthritis and MUScle (RAMUS) Study: Protocol for an observational single-arm study of skeletal muscle in patients with rheumatoid arthritis receiving tofacitinib.

Bennett, Joshua L / Egail, Maha / Anderson, Amy E / Dodds, Richard / Feeney, Catherine / Gorman, Gráinne S / Pratt, Arthur G / Sayer, Avan A / Hollingsworth, Kieren G / Isaacs, John D

Journal of frailty, sarcopenia and falls

2023 Volume 8, Issue 1, Page(s) 53–59

Abstract: People with rheumatoid arthritis (RA) are disproportionately affected by sarcopenia, the generalised loss of muscle strength and mass, consequently facing an increased risk of falls, functional decline and death. Currently, there are no approved ... ...

Abstract	People with rheumatoid arthritis (RA) are disproportionately affected by sarcopenia, the generalised loss of muscle strength and mass, consequently facing an increased risk of falls, functional decline and death. Currently, there are no approved pharmacological treatments for sarcopenia. RA patients who start tofacitinib (a Janus kinase inhibitor) develop small increases in serum creatinine that are not explained by renal function changes and could reflect sarcopenia improvement. The RAMUS Study is a proof of concept, single-arm observational study in which patients with RA who commence tofacitinib according to routine care will be offered participation according to eligibility criteria. Participants will undergo lower limb quantitative magnetic resonance imaging, whole-body dual energy x-ray absorptiometry, joint examination, muscle function testing and blood tests at three time points: prior to starting tofacitinib and 1 and 6 months afterwards. Muscle biopsy will be performed before and 6 months after starting tofacitinib. The primary outcome will be lower limb muscle volume changes following treatment initiation. The RAMUS Study will investigate whether muscle health improves following tofacitinib treatment for RA. Identifying a potential pharmacological treatment for sarcopenia could have important implications for individuals with RA and for older people in general. ISRCTN registry ID: 13364395.
Language	English
Publishing date	2023-03-01
Publishing country	Greece
Document type	Journal Article
ISSN	2459-4148
ISSN (online)	2459-4148
DOI	10.22540/JFSF-08-053
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Article ; Online: Delivery of loaded MR1 monomer results in efficient ligand exchange to host MR1 and subsequent MR1T cell activation.

Communications biology

2024 Volume 7, Issue 1, Page(s) 228

Abstract: MR1-restricted T cells have been implicated in microbial infections, sterile inflammation, wound healing and cancer. Similar to other antigen presentation molecules, evidence supports multiple, complementary MR1 antigen presentation pathways. To ... ...

Abstract	MR1-restricted T cells have been implicated in microbial infections, sterile inflammation, wound healing and cancer. Similar to other antigen presentation molecules, evidence supports multiple, complementary MR1 antigen presentation pathways. To investigate ligand exchange pathways for MR1, we used MR1 monomers and tetramers loaded with 5-(2-oxopropylideneamino)-6-d-ribitylaminouracil (5-OP-RU) to deliver the antigen. Using MR1-deficient cells reconstituted with wild-type MR1 or MR1 molecules that cannot bind 5-OP-RU, we show that presentation of monomer-delivered 5-OP-RU is dependent on cellular MR1 and requires the transfer of ligand from the soluble molecule onto MR1 expressed by the antigen presenting cell. This mode of antigen delivery strengthens the evidence for post-ER ligand exchange pathways for MR1, which could represent an important avenue by which MR1 acquires antigens derived from endocytosed pathogens.
MeSH term(s)	Histocompatibility Antigens Class I/metabolism ; Lymphocyte Activation ; Ligands ; Antigen Presentation ; Antigens/metabolism ; Ribitol/analogs & derivatives ; Uracil/analogs & derivatives
Chemical Substances	Histocompatibility Antigens Class I ; 5-(2-oxopropylideneamino)-6-d-ribitylaminouracil ; Ligands ; Antigens ; Ribitol (488-81-3) ; Uracil (56HH86ZVCT)
Language	English
Publishing date	2024-02-24
Publishing country	England
Document type	Journal Article
ISSN	2399-3642
ISSN (online)	2399-3642
DOI	10.1038/s42003-024-05912-4
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Article: Broad de-regulated U2AF1 splicing is prognostic and augments leukemic transformation via protein arginine methyltransferase activation.

bioRxiv : the preprint server for biology

2024

Abstract: The role of splicing dysregulation in cancer is underscored by splicing factor mutations; however, its impact in the absence of such rare mutations is poorly understood. To reveal complex patient subtypes and putative regulators of pathogenic splicing in ...

Abstract	The role of splicing dysregulation in cancer is underscored by splicing factor mutations; however, its impact in the absence of such rare mutations is poorly understood. To reveal complex patient subtypes and putative regulators of pathogenic splicing in Acute Myeloid Leukemia (AML), we developed a new approach called OncoSplice. Among diverse new subtypes, OncoSplice identified a biphasic poor prognosis signature that partially phenocopies
Language	English
Publishing date	2024-02-08
Publishing country	United States
Document type	Preprint
DOI	10.1101/2024.02.04.578798
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Article ; Online: Paralog-specific signaling by IRAK1/4 maintains MyD88-independent functions in MDS/AML.

Bennett, Joshua / Ishikawa, Chiharu / Agarwal, Puneet / Yeung, Jennifer / Sampson, Avery / Uible, Emma / Vick, Eric / Bolanos, Lyndsey C / Hueneman, Kathleen / Wunderlich, Mark / Kolt, Amal / Choi, Kwangmin / Volk, Andrew / Greis, Kenneth D / Rosenbaum, Jan / Hoyt, Scott B / Thomas, Craig J / Starczynowski, Daniel T

Blood

2023 Volume 142, Issue 11, Page(s) 989–1007

Abstract: Dysregulation of innate immune signaling is a hallmark of hematologic malignancies. Recent therapeutic efforts to subvert aberrant innate immune signaling in myelodysplastic syndrome (MDS) and acute myeloid leukemia (AML) have focused on the kinase IRAK4. ...

Abstract	Dysregulation of innate immune signaling is a hallmark of hematologic malignancies. Recent therapeutic efforts to subvert aberrant innate immune signaling in myelodysplastic syndrome (MDS) and acute myeloid leukemia (AML) have focused on the kinase IRAK4. IRAK4 inhibitors have achieved promising, though moderate, responses in preclinical studies and clinical trials for MDS and AML. The reasons underlying the limited responses to IRAK4 inhibitors remain unknown. In this study, we reveal that inhibiting IRAK4 in leukemic cells elicits functional complementation and compensation by its paralog, IRAK1. Using genetic approaches, we demonstrate that cotargeting IRAK1 and IRAK4 is required to suppress leukemic stem/progenitor cell (LSPC) function and induce differentiation in cell lines and patient-derived cells. Although IRAK1 and IRAK4 are presumed to function primarily downstream of the proximal adapter MyD88, we found that complementary and compensatory IRAK1 and IRAK4 dependencies in MDS/AML occur via noncanonical MyD88-independent pathways. Genomic and proteomic analyses revealed that IRAK1 and IRAK4 preserve the undifferentiated state of MDS/AML LSPCs by coordinating a network of pathways, including ones that converge on the polycomb repressive complex 2 complex and JAK-STAT signaling. To translate these findings, we implemented a structure-based design of a potent and selective dual IRAK1 and IRAK4 inhibitor KME-2780. MDS/AML cell lines and patient-derived samples showed significant suppression of LSPCs in xenograft and in vitro studies when treated with KME-2780 as compared with selective IRAK4 inhibitors. Our results provide a mechanistic basis and rationale for cotargeting IRAK1 and IRAK4 for the treatment of cancers, including MDS/AML.
MeSH term(s)	Humans ; Interleukin-1 Receptor-Associated Kinases/genetics ; Interleukin-1 Receptor-Associated Kinases/metabolism ; Myeloid Differentiation Factor 88/genetics ; Myeloid Differentiation Factor 88/metabolism ; Proteomics ; Signal Transduction ; Myelodysplastic Syndromes/drug therapy ; Myelodysplastic Syndromes/genetics ; Leukemia, Myeloid, Acute/genetics
Chemical Substances	Interleukin-1 Receptor-Associated Kinases (EC 2.7.11.1) ; Myeloid Differentiation Factor 88 ; IRAK1 protein, human (EC 2.7.11.1)
Language	English
Publishing date	2023-05-13
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	80069-7
ISSN	1528-0020 ; 0006-4971
ISSN (online)	1528-0020
ISSN	0006-4971
DOI	10.1182/blood.2022018718
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Article: CD5 Deficiency Alters Helper T Cell Metabolic Function and Shifts the Systemic Metabolome.

Whitley, Kiara V / Freitas, Claudia M Tellez / Moreno, Carlos / Haynie, Christopher / Bennett, Joshua / Hancock, John C / Cox, Tyler D / Pickett, Brett E / Weber, K Scott

Biomedicines

2022 Volume 10, Issue 3

Abstract: Metabolic function plays a key role in immune cell activation, destruction of foreign pathogens, and memory cell generation. As T cells are activated, their metabolic profile is significantly changed due to signaling cascades mediated by the T cell ... ...

Abstract	Metabolic function plays a key role in immune cell activation, destruction of foreign pathogens, and memory cell generation. As T cells are activated, their metabolic profile is significantly changed due to signaling cascades mediated by the T cell receptor (TCR) and co-receptors found on their surface. CD5 is a T cell co-receptor that regulates thymocyte selection and peripheral T cell activation. The removal of CD5 enhances T cell activation and proliferation, but how this is accomplished is not well understood. We examined how CD5 specifically affects CD4+ T cell metabolic function and systemic metabolome by analyzing serum and T cell metabolites from CD5WT and CD5KO mice. We found that CD5 removal depletes certain serum metabolites, and CD5KO T cells have higher levels of several metabolites. Transcriptomic analysis identified several upregulated metabolic genes in CD5KO T cells. Bioinformatic analysis identified glycolysis and the TCA cycle as metabolic pathways promoted by CD5 removal. Functional metabolic analysis demonstrated that CD5KO T cells have higher oxygen consumption rates (OCR) and higher extracellular acidification rates (ECAR). Together, these findings suggest that the loss of CD5 is linked to CD4+ T cell metabolism changes in metabolic gene expression and metabolite concentration.
Language	English
Publishing date	2022-03-18
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2720867-9
ISSN	2227-9059
ISSN	2227-9059
DOI	10.3390/biomedicines10030704
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Article ; Online: Paradoxical Effects of Endoplasmic Reticulum Aminopeptidase 1 Deficiency on HLA-B27 and Its Role as an Epistatic Modifier in Experimental Spondyloarthritis.

Tran, Tri M / Gill, Tejpal / Bennett, Joshua / Hong, Sohee / Holt, Vance / Lindstedt, Anders J / Bakshi, Sufia / Sikora, Keith / Taurog, Joel D / Breban, Maxime / Navid, Fatemeh / Colbert, Robert A

Arthritis & rheumatology (Hoboken, N.J.)

2022 Volume 75, Issue 2, Page(s) 220–231

Abstract: Objective: We undertook this study to examine the functional basis for epistasis between endoplasmic reticulum aminopeptidase 1 (ERAP1) and HLA-B27 in experimental spondyloarthritis (SpA).: Methods: ERAP1-knockout rats were created using genome ... ...

Abstract	Objective: We undertook this study to examine the functional basis for epistasis between endoplasmic reticulum aminopeptidase 1 (ERAP1) and HLA-B27 in experimental spondyloarthritis (SpA). Methods: ERAP1-knockout rats were created using genome editing and bred with HLA-B27/human β Results: ERAP1 deficiency increased the ratio of folded to unfolded (β Conclusion: ERAP1 deficiency reduced HLA-B27 misfolding and improved folding while having opposing effects on HLA-B7. The finding that HLA-B27-Tg rats had partial protection against SpA in this study is consistent with genetic evidence that loss-of-function and/or reduced expression of ERAP1 reduces the risk of ankylosing spondylitis. Functional studies support the concept that the effects of ERAP1 on HLA-B27 and SpA may be a consequence of how peptides affect the biology of this allotype rather than their role as antigenic determinants.
MeSH term(s)	Animals ; Humans ; Rats ; Aminopeptidases/genetics ; Aminopeptidases/metabolism ; Endoplasmic Reticulum/metabolism ; HLA-B27 Antigen/genetics ; HLA-B27 Antigen/metabolism ; HLA-B7 Antigen ; Minor Histocompatibility Antigens/genetics ; Spondylitis, Ankylosing/genetics ; Arthritis/genetics ; Arthritis/metabolism
Chemical Substances	Aminopeptidases (EC 3.4.11.-) ; ERAP1 protein, human (EC 3.4.11.-) ; HLA-B27 Antigen ; HLA-B7 Antigen ; Minor Histocompatibility Antigens
Language	English
Publishing date	2022-12-28
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, N.I.H., Intramural
ZDB-ID	2756371-6
ISSN	2326-5205 ; 2326-5191
ISSN (online)	2326-5205
ISSN	2326-5191
DOI	10.1002/art.42327
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