Knowledge and motivations of training in peer review: An international cross-sectional survey.

BACKGROUND: Despite having a crucial role in scholarly publishing, peer reviewers do not typically require any training. The purpose of this study was to conduct an international survey on the current perceptions and motivations of researchers regarding peer review training. METHODS: A cross-sectional online survey was conducted of biomedical researchers. A total of 2000 corresponding authors from 100 randomly selected medical journals were invited via email. Quantitative items were reported using frequencies and percentages or means and SE, as appropriate. A thematic content analysis was conducted for qualitative items in which two researchers independently assigned codes to the responses for each written-text question, and subsequently grouped the codes into themes. A descriptive definition of each category was then created and unique themes-as well as the number and frequency of codes within each theme-were reported. RESULTS: A total of 186 participants completed the survey of which 14 were excluded. The majority of participants indicated they were men (n = 97 of 170, 57.1%), independent researchers (n = 108 of 172, 62.8%), and primarily affiliated with an academic organization (n = 103 of 170, 62.8%). A total of 144 of 171 participants (84.2%) indicated they had never received formal training in peer review. Most participants (n = 128, 75.7%) agreed-of which 41 (32.0%) agreed strongly-that peer reviewers should receive formal training in peer review prior to acting as a peer reviewer. The most preferred training formats were online courses, online lectures, and online modules. Most respondents (n = 111 of 147, 75.5%) stated that difficulty finding and/or accessing training was a barrier to completing training in peer review. CONCLUSION: Despite being desired, most biomedical researchers have not received formal training in peer review and indicated that training was difficult to access or not available.

Limited online training opportunities exist for scholarly peer reviewers.

OBJECTIVES: To create a comprehensive list of all openly available online trainings in scholarly peer review and to analyze their characteristics. STUDY DESIGN AND SETTING: A systematic review of online training material in scholarly peer review openly accessible between 2012 and 2022. Training characteristics were presented in evidence tables and summarized narratively. A risk of bias tool was purpose-built for this study to evaluate the included training material as evidence-based. RESULTS: Fourty-two training opportunities in manuscript peer review were identified, of which only twenty were openly accessible. Most were online modules (n = 12, 60%) with an estimated completion time of less than 1 hour (n = 13, 65%). Using our ad hoc risk of bias tool, four sources (20%) met our criteria of evidence-based. CONCLUSION: Our comprehensive search of the literature identified 20 openly accessible online training materials in manuscript peer review. For such a crucial step in the dissemination of literature, a lack of training could potentially explain disparities in the quality of scholarly publishing.

TREM2 Promotes Immune Evasion by Mycobacterium tuberculosis in Human Macrophages.

Macrophage surface receptors are critical for pathogen defense, as they are the gatekeepers for pathogen entry and sensing, which trigger robust immune responses. TREM2 (triggering receptor expressed on myeloid cells 2) is a transmembrane surface receptor that mediates anti-inflammatory immune signaling. A recent study showed that TREM2 is a receptor for mycolic acids in the mycobacterial cell wall and inhibits macrophage activation. However, the underlying functional mechanism of how TREM2 regulates the macrophage antimycobacterial response remains unclear. Here, we show that Mycobacterium tuberculosis, the causative agent for tuberculosis, specifically binds to human TREM2 to disable the macrophage antibacterial response. Live but not killed mycobacteria specifically trigger the upregulation of TREM2 during macrophage infection through a mechanism dependent on STING (the stimulator of interferon genes). TREM2 facilitated uptake of M. tuberculosis into macrophages and is responsible for blocking the production of tumor necrosis factor alpha (TNF-α), interleukin-1ß (IL-1ß), and reactive oxygen species (ROS), while enhancing the production of interferon-ß (IFN-ß) and IL-10. TREM2-mediated blockade of ROS production promoted the survival of M. tuberculosis within infected macrophages. Consistent with this, genetic deletion or antibody-mediated neutralization of TREM2 reduced the intracellular survival of M. tuberculosis through enhanced production of ROS. Importantly, inhibition of type I IFN signaling in TREM2-overexpressing macrophages restored the ability of these cells to produce inflammatory cytokines and ROS, resulting in normal levels of intracellular bacteria killing. Collectively, our study identifies TREM2 as an attractive host receptor for host-directed antimycobacterial therapeutics. IMPORTANCE Mycobacterium tuberculosis is one of the most ancient bacterial pathogens and remains the leading cause of death from a single bacterial agent. The success of M. tuberculosis relies greatly on its ability to parasitize and disable its host macrophages. Previous studies have found that M. tuberculosis uses its unique cell wall lipids to manipulate the immune response by binding to specific surface receptors on macrophages. Our study reveals that M. tuberculosis binds to TREM2, an immunomodulatory receptor expressed on macrophages, to facilitate a "silent" mode of entry. Increased levels of TREM2 triggered by intracellular sensing of M. tuberculosis promoted the intracellular survival of M. tuberculosis through type I IFN-driven inhibition of reactive oxygen species (ROS) and proinflammatory cytokine production. Importantly, deletion of TREM2 reversed the effects of "silent" entry and resulted in increased production of inflammatory cytokines, generation of ROS, and cell death. As such, antibody-mediated or pharmacological targeting of TREM2 could be a promising strategy for novel treatments against M. tuberculosis infection.