bluuebunny/crossref_metadata_2025_split huggingface dataset:
Female minority students-plight of staying alive in education during an unending pandemic!
Authors: Fazal Nadeem , Nguyen Minh-Thu , Simmons Jazmyne Durrah , Olk Sandra , Jhatu Prabjyot 
Published: January 2023

Abstract
COVID-19 pandemic laid bare deep inequalities and inequities. Disruptions brought to light by the ongoing pandemic are exacerbating risks and vulnerabilities both within education careers and personal lives. Widespread economic, sociological, and psychological damage has challenged female minority students in education more than their male counterparts. We surveyed female minority students as compared to male students at Chicago State University and found mixed ideas and opinions. The concerns on top of the list were fear of contracting COVID-19, existential epiphanies, and poor study conditions. More women, conditioned to design their lives around education are not enrolling for educational opportunities. One reason is that they can’t find childcare; another is they struggle with education/life balance. It’s not one cause but the pandemic has made it complex and multi-faceted. For other students, the pandemic offered many new opportunities that were practically never heard off. Some of the most common perks were, i.e., the ability to study remotely from anywhere, cutting out big city commutes, being able to give peak time to family, and greater flexibility in setting daily chores. A common theme for most of the surveyed students was that changes forced by the current pandemic are playing out a new social justice awakening on college campuses especially minority institutions like Chicago State University. Overarching suggestion was that right decisions made today in the context of a pandemic will have long-term consequences for the future of education. Overwhelming minority students proposed a faculty mentor and a peer-mentor to address the academic advising as well as personal guide to facilitate upheavals in pandemic situations.
Is it not over yet? – pandemic-induced ongoing burn out continues for students in Azerbaijan.
Authors: Fazal Nadeem , Cebiyev Nihat , Alakbarova Gulgaz , Huseynbayli Ayshan , Garajayev Azer , Safarova Arzu Safarova 
Published: January 2023

Abstract
In a nagging pandemic, while there will be some regression when the dust from pandemic settles, online, remote and hybrid education seems to stay for good and is expected to maintain a substantial portion of education. Students chronic burnout continues with more questions raised every day than the answers and promises made. It is a known psychological fact that when a younger generation of students encounters life-threatening events, they tend to reflect on death and uncertainty and take stock of their lives with defining what to make of their lives and how to achieve that. We surveyed mental health, social life and its impact on academics of medical and engineering students in Azerbaijan and reported the following data. Out of 274 respondents were 51% female and 48.2% male. 86.5% were from the age group (18–25) and 12.5% from (25–35) years. Majority of the students found themselves juggling with too many balls at the same time, not everyone could keep the focus, skill set and training to succeed. Female students delayed their cultural-ordained marriageable age in pursuit of a well-settled career partner, while male students found themselves looking for an alternative career path. Majority of professional students burn-out by a loss of at least two years of their professional education. This seemed to play out more for medical students as they were not able to find experiential training and hospital residencies. This included medical and engineering students who were ambitious to seek western education but lockdowns and visa regulations held them hostage at their home countries. Azerbaijan students however, were resilient enough to withstand the dual trauma of war with their neighboring country while fighting a global war against COVID-19 pandemic.
Evidence-based learning modules and culturally responsive mentoring to engage underserved undergraduate students
Authors: Mishra Manoj K 
Published: January 2023

Abstract
The number of underrepresented minorities in the biomedical workforce has quadrupled over the past three decades, yet doctoral-level minority scientists still make up less than 5% of the total workforce. Thus, it is imperative to implement strategies to maintain the degree and diversity of scientific research and education expertise in biomedical disciplines. In this study, we develop, deploy, and assess the effectiveness of immunology learning by integrating evidence-based learning (EBL) modules to engage and motivate underserved students. Additionally, we provided robust culturally responsive mentoring to engage students in immunology education and research. Our initial finding demonstrates that EBL modules enhanced the collaborative learning and research activities and broadened their understanding of immunological problems. Therefore, our study suggests that a) implementing EBL modules in the immunology curriculum and b) engaging students through in-person mentoring during classroom engagement, attract and sustain underrepresented minority students to the immunology courses, improve undergraduate research training, and enhance educational appetite in biomedical disciplines.
Supported by grants from NIH UO1GM132769 and NSF 1912322.
Thymic Interferon Impacts T cell Selection
Authors: Ashby Katherine Maude , Martinez Ryan J , Salgado Oscar C , Hogquist Kristin Ann 
Published: January 2023

Abstract
Autoimmune diseases are triggered by the loss of immunological tolerance to self-antigens. Although previous work has characterized mechanisms driving immune tolerance to tissue restricted self-antigens, less is understood about how tolerance is established for inflammation-associated self-antigens that are expressed transiently during acute infection. This is particularly important with the discovery that autoantibodies to type I interferons (IFN) are commonly found in elderly individuals, and predispose to severe COVID19. Recent work from several groups has found that Type I and Type III IFN are expressed in the thymus at steady state (in the absence of infection) and drive expression of interferon stimulated genes in antigen presenting cells and developing thymocytes. We hypothesize that IFN is present in the thymus in order to tolerize developing T cells to self-antigens presented during acute infection (such as those derived from interferon and interferon stimulated genes.) In line with this, T cell receptor (TCR) repertoire analysis showed that mice lacking the type I IFN receptor (Ifnar KO) have distinct T conventional (Tconv) and T regulatory (Treg) TCR repertoires from wild type (WT) mice. We have identified two groups of interesting receptors from this TCR repertoire analysis; 1) IFN-deleted receptors(~50 TCRs) that are present in the Ifnar KO Tconv repertoire and absent from the WT repertoire, and 2) IFN-dependent Treg receptors(~750 TCRs) that are present in the WT Treg repertoire but lost from the Ifnar KO Treg repertoire. We have expressed TCRs from each group in hybridomas and retrogenic mice in order to determine the specificity of these TCRs and characterize the development of thymocytes expressing them.
Supported by grants from NIH (T32 AI007313)
Single-cell proteogenomics reveals that SLAM/SAP signaling regulates the development of innate-like γδ T cell subsets with distinct TCR repertoires
Authors: Boyson Jonathan E , Andretta Emma , Hampel Kenneth J , Sidiropoulos Nikoletta , Dienz Oliver , Majumdar Devdoot , Mistri Somen 
Published: January 2023

Abstract
γδ T cells are non-conventional T cells that are highly enriched in the mucosal tissues where they play critical roles in immunity. We recently demonstrated that the SLAM/SAP signaling pathway regulates the thymic development of innate-like γδT17 and γδTIFN subsets, in addition to γδNKT cells. Here, we utilized a single-cell proteogenomics approach coupled with γδ V(D)J profiling to define the transcriptional landscape and developmental checkpoints of SAP-dependent γδ T cells. This analysis not only confirmed our previous finding that SLAMF1 and SLAMF6 expression marks γδT17 and γδTIFN subsets, respectively, it also identified SLAMF7 as a novel marker of the SAP-dependent innate-like CD44+ CD45RB+ γδTIFN cells in both the thymus and periphery. Next, our data indicated that disruption of SAP-dependent signaling impaired γδT17 development at a very early (CD24high CD73−) stage, and was associated with the decreased expression of critical regulators of γδT17 development such as Blk and c-Maf. In contrast, while SAP also impaired γδTIFN development at an early (CD24high CD73+) stage, SAP-deficient γδTIFN cells exhibited increased expression of genes associated with TCR signaling and thymic export such as Prkch, Dgka, Klf2, and S1p1r. Finally, our analysis revealed significant alterations in the γδT17 TCR repertoire in both embryonic/neonatal thymus and the lung, as well as the presence of a SAP-dependent IFN-γ-producing lung Vγ4 population that preferentially utilized TRDV7. Altogether, these data suggest that SLAM/SAP signaling acts during the very early stages of γδ T cell development where it regulates critical pathways in both γδT17 and γδTIFN development, and influences the development of the innate-like γδ TCR repertoire.
Supported by NIH (R03AI153902, P30GM118228), AAI Careers in Immunology Fellowship
Collaboration between Osteopontin and Macrophage Migration Inhibitory Factor in Autoimmune Myocarditis
Authors: Medrano Megan T , Nalawade Saisha , Huizar Carol Chase , Yuhara Alec , Forsthuber Thomas G 
Published: January 2023

Abstract
Macrophage migration inhibitory factor (MIF) is a pro-inflammatory cytokine elevated in multiple conditions. MIF is also elevated in autoimmune myocarditis (AM), a condition in which the immune system aberrantly attacks the heart muscle. AM can be induced by antigenic mimicry, autoimmune stimulation, genetic defects, issues with regulatory T cells, dysregulation of immune effector cells. AM also has the possibility to progress to the fatal disease dilated cardiomyopathy (DCM) through chronic inflammation, the deposition and crosslinking of collagen, proliferation by fibroblasts, and differentiation into myofibroblasts. Our lab has previously shown that MIF and OPN synergize to enhance the progression of disease to DCM, by affecting cardiac fibrosis and the deposition of collagen. Glucocorticoids (GCs) are given to suppress the inflammation caused by immune reactions and therefore are prescribed as treatment for autoimmune myocarditis. However, GCs are unable prevent the progression of AM to DCM. Our lab investigated the role of GCs for promoting the actions of MIF by enhancing the OPN-dependent deposition of collagen in the myocardium by gene expression of extracellular matrix proteins affected by AM through qPCR and their protein concentration by ELISA. Establishing a pathway for collagen deposition in AM will allow for the development of more effective treatment and prevention of the progression to DCM.
Archived antigen boosts CD8 T cell memory responses during an unrelated infection.
Authors: Doan Thu A , Tamburini Beth 
Published: January 2023

Abstract
Numerous studies have shown viral antigens can persist in lymph nodes after the resolution of the infection. We showed that lymphatic endothelial cells (LECs), which comprise the lymphatic vasculature, are the predominant cell type required for the persistence of antigen within the lymph node. We termed this process antigen archiving due to the ability of LECs to actively acquire and store antigens to which an active immune response occurred. This process involves antigen acquisition, retention, and exchange of the antigen between LECs and dendritic cells, resulting in the presentation of the archived antigens to CD8 memory T cells and improving effector function. In more recent data, we demonstrated that LEC death causes the release of archived antigens during LN contraction. We found that archived antigens could be released during an unrelated viral infection, during the time frame of LEC death. This release of antigen was visualized by a significant increase in archived antigen-specific endogenous or transferred memory CD8 T cells, but not memory T cells of an unrelated specificity. The increase in archived antigen-specific CD8 T cells maintained a more effector-like phenotype and performed significantly better upon antigenic challenge with Listeria monocytogenes (LM) expressing ovalbumin. Mice that received an unrelated infection 2–3 weeks prior to antigenic challenge demonstrated improved protection against LM-ova. In conclusion, archived antigen release during a secondary unrelated infection boosts the archived antigen-specific memory CD8 T cell population. These findings bring into question whether some previous data demonstrating heterologous immunity may be a result of archived antigen release.
Supported by R01 AI121209 R21 AI155929
The anti-inflammatic activity of a sulfated polysaccharide Fucoidan in innate immune cells
Authors: Miyazaki Yoshiyuki , Satoyama Toshiya , Nakano Hayato , Takeuchi Shugo , Takeuchi Hideaki , Tachikawa Daisuke 
Published: January 2023

Abstract
Fucoidan is a series of natural sulfated polysaccharides derived from brown seaweeds and have reported to possess various biological activities such as anti-tumor, anti-virus, and immuno-modulatory effects. In previous study, we revealed that fucoidan derived from Cladosiphon okamuranus activated murine macrophage-like cell line RAW264 cooperatively with Zymosan, a Saccharomyces cerevisiae-derived β-glucan. On the other hand, several reports demonstrated that fucoidan inhibited lipopolysaccharide (LPS)-induced production of nitrogen oxide (NO) and inflammatory cytokines by RAW264 cells. Therefore, in this study, we investigated the potential of fucoidan derived from Undaria pinnatifida to regulate the excessive activation of RAW264 cells in response to overstimulation with pathogen components. RAW264 cells were inoculated at 20000 cells/well in 96-well culture plates, and after a recovery culture for 24 hr, the cells were treated with fucoidan with or without appropriate concentrations of each ligand for pattern recognition receptors (PRRs) including Toll-like receptors (TLRs). Whereas the production of NO was significantly enhanced with fucoidan alone, it was dose-dependently inhibited by fucoidan under stimulation with Pam3CSK4 (TLR1/TLR2 ligand), heat killed Listeria monocytogenes (HKLM, TLR2 ligand), LPS (TLR4 ligand), Pam2CGDPKHPKSF (FSL-1, TLR2/TLR6 ligand). These results suggested that fucoidan have beneficial ability to alleviate excessive inflammatory reaction during pathogenic infection and maintain suitable immune balance.
Supported by Laboratory of Analytical Food Immunoscience belonging YM is a donated fund laboratory established in Faculty of Agriculture, Kyushu University by Ventuno Co., Ltd.
THC decreases bone marrow-derived macrophage activation in a dose-dependent manner
Authors: Carter Taylor H , Nagarkatti Mitzi , Nagarkatti Prakash 
Published: January 2023

Abstract
Macrophage activation is a major factor in progressive illnesses such as atherosclerosis, arthritis, and HIV-associated Neurological Disorder (HAND). Δ9-Tetrahydrocannabinol (THC), the main psychoactive compound found in cannabis, has been shown to have beneficial effects in treating these diseases, although the mechanism of action is not clear. Our lab and others have demonstrated the role of THC as an anti-inflammatory agent. In the current study, we attempted to investigate the effect of THC on macrophage activation. For this purpose, bone marrow was collected from tibia and femurs of C57BL/6 mice (10–12 weeks) and cells cultured in presence of macrophage colony stimulating factor (MCSF) for 4 days, in order to induce macrophage differentiation. On day 4, Lipopolysaccharide (LPS), gp120 of HIV or vehicle was added to the cultures and flow cytometry performed. Our results showed that THC treatment decreased F4/80+ macrophages in both LPS and gp120 groups in a dose-dependent manner when compared to vehicle-treated controls. MicroRNA-sequencing analysis showed a large number of miRs were dysregulated several fold. Importantly, there was an increase in the THC group of various miRNA such as miR-2137 and miR-486-5p that are involved in cell development and proliferation. Together, the role of THC in decreasing bone marrow-derived activated macrophages through miR dysregulation could provide new treatment strategies for diseases such as atherosclerosis, arthritis, and HAND.
Supported by NIH grants P01AT003961, P20GM103641, R01ES030144, R01AI129788, R01AI123947 and R01AI160896
Inhibition of Glycolysis Modifies Distinctive Metabolic and Immune Pathways Across Multiple Tissue Compartments Associated with B and T Follicular Helper Cells
Authors: Wells Ann , Wilson John , Roopenian Derry C , Chang Chih-Hao , Carter Gregory 
Published: January 2023

Abstract
Systemic lupus erythematosus (SLE) is the most common form of lupus; however, only one new drug was approved for SLE in the last 60 years. Inhibition of glycolysis via 2-deoxyglucose (2DG), a competitive inhibitor of glucose-6-phosphate, has recently shown efficacy in attenuating tumor growth and reducing autoimmune pathology; however, the mechanism of this efficacy is somewhat unclear. To elucidate how 2DG longitudinally modulates pathways within the context of systemic lupus erythematosus (SLE), BXSB.YaaIL15−/−,CD8−/− mice, an SLE model, were treated orally with 2DG for 96-hours or 4-weeks, after which the transcriptional profiles of 9 tissues (heart, hippocampus, hypothalamus, kidney, liver, prefrontal cortex, skeletal muscle, small intestine, and spleen) were analyzed using unsupervised clustering and weighted gene correlation network analysis. Principal component analysis showed mice clustered by tissue. Tissues correlated to B cells and T follicular helper cells grouped together according to their summary gene expression for modules treatment or treatment, in a time dependent manner, and three pathway groups, transcription, immune, and glucose, emerged. However, within each tissue cluster, pathways for each module were uniquely altered by treatment or treatment, in a time dependent manner, according to ANOVA. Furthermore, while most pathways identified were grouped into either immune or metabolic, there was little overlap of specific pathways identified between tissues. These results show that 2DG has a systemic impact altering immune and metabolic pathways, but in a tissue-specific manner. Ongoing work includes identifying genes that are potentially central to pathway alterations for follow-up analysis.
Supported by the AAI Intersect Fellowship
An immunomodulatory human commensal coordinately regulates inflammatory and metabolic disease
Authors: Tan Chin Yee , Surana Neil 
Published: January 2023

Abstract
Specific members of the microbiota are known to modulate the immune system, which also plays an important role in regulating metabolism. Indeed, there are emerging data detailing specific bacterial species that impact multiple physiological outcomes, but the mechanisms underlying these pleiotropic effects are unclear. We previously discovered a new human commensal bacteria species, Clostridium immunis, that protects against colitis. Here, we define the host and bacterial mechanisms of action for C. immunis-mediated disease regulation. We found that C. immunis treatment decreases ILC3 numbers and function in mice and humans. Consistent with this finding, C. immunis regulates the severity of intestinal and extra-intestinal inflammatory diseases, as well as body composition in an ILC3-dependent manner. Interestingly, C. immunis influences metabolism by decreasing expression of lipid processing genes, thereby inhibiting dietary fat processing. The bioactive component of C. immunis is a secreted product and comparative genomics identified 8 C. immunis genes associated with ILC3 regulation. Collectively, we have demonstrated how a single bacterial species impacts different physiological pathways via its suppression of ILC3s. More broadly, our work reveals a microbiome-based therapy for diseases driven by pathogenic ILC3s.
Supported by a Development Award from the National University of Singapore and a Graduate Student Award from the Triangle Center for Evolutionary Medicine
Rab27A-dependent transfer of CD11c+ cell exosomes regulate gut immunity
Authors: Bauer Kaylyn , Round June , O’Connell Ryan M 
Published: January 2023

Abstract
Intercellular communication is critical for maintaining homeostasis in mammalian organ systems, including the gastrointestinal (GI) tract. Exosomes are small nanoscale lipid extracellular vesicles that mediate communication between a wide variety of cell types. Notably, the roles played by immune cell exosomes in regulating homeostasis and inflammation in the GI tract are largely uncharacterized. Here, we describe an unknown mechanism of exosome-mediated immune regulation within the GI tract. By generating novel mouse strains, we demonstrate that disruption of exosome signaling via the deletion of Rab27a in CD11c+ myeloid cells exacerbates colitis, which is reversed through administration of dendritic cell (DC)-derived exosomes. Profiling small noncoding RNAs within exosomes from colonic tissues revealed a distinct subset of microRNAs (miRNAs) carried by both gut- and DC-derived exosomes. Among the DC-enriched exosomal miRNAs, miR-146a was transferred from gut CD11c+ cells to myeloid and T cells through a Rab27-dependent mechanism to decrease macrophage-mediated inflammation during colitis. Clinically, RAB27A is also expressed at lower levels in a cohort of ulcerative colitis patients versus healthy controls. Together, this work reveals an exosome-mediated modulatory mechanism of gut inflammation, paving the way for exosomes containing miRNA cargo as a potential therapeutic for inflammatory bowel disease.
Supported by National Institutes of Health Grants T32 AI 138945-1 (K.M.B.) and AI123106-01A1 (R.M.O.)