Matching Items (26)
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- All Subjects: Immunology
- Creators: School of Life Sciences
- Member of: Barrett, The Honors College Thesis/Creative Project Collection
Description
As a child with eyes wide open to the wonders of the universe, my enthusiasm for science often met the obstacle of scarcity—there were hardly any science-focused children's books that spoke in a language that a curious mind like mine could truly relish. It is from this personal quest for knowledge that the seed for this book was planted. My ambition has been to craft an adventure in immunology that I wished for in my youth—a tale where science is as gripping as any fable or fantasy. In creating Bodyville, a bustling city within the human body, and telling the tales of Mia, the neutrophil and her fellow cellular defenders, I have endeavored to forge a connection between young readers and the marvels of the immune system. This narrative is not a mere accumulation of facts; it is a door to a universe where learning is living, and science is storytelling. The methodology behind this book is as purposeful as it is personal. Utilizing my younger cousin and his classmates as a lens through which I could gauge understanding and excitement, I conducted informal focus groups to refine both the visuals and the narrative arc. Their reactions and comprehension shaped the course of Bodyville's tale, ensuring that the content resonated with the target audience of 6-8 -year-olds. To construct the world of Bodyville with scientific integrity and imaginative flair, I turned to a wealth of scientific texts, distilling complex immunological concepts into digestible pieces that form the backbone of our story. I then used Dall-E AI, an innovative artificial intelligence program, to transform detailed descriptions of each scene into captivating visuals through prompt engineering. The resulting illustrations are not just images; they are windows into the heroic deeds of Mia and her companions. By intertwining accurate science with narrative and visual artistry, this book serves a dual purpose. It aims to illuminate the silent guardians within our bodies while fostering a relationship between young readers and the science that shapes their health and well-being. This is a journey through Bodyville that goes beyond education—it’s an expedition that equips young minds with knowledge and envelops them in the excitement of discovery. So, let us embark on this unique voyage. Welcome to Bodyville, where science meets story, and the smallest of heroes engage in the mightiest of battles, leading us page by page to a deeper understanding of the immune system’s mysteries.
ContributorsMadaan, Rohan (Author) / Florsheim, Esther (Thesis director) / Salamone, Damien (Committee member) / Barrett, The Honors College (Contributor) / School of Life Sciences (Contributor)
Created2024-05
Description
Adaptive therapy is a novel up-and-coming cancer treatment strategy to minimize chemoresistance in cells to improve patient prognosis. The standard of care cancer treatment has a fixed linear approach known as Maximum Tolerated Dose (MTD) which promotes an exponential growth of resistant cancer cell populations in the tumor. Through this treatment procedure, a population of chemoresistant cells resurges, decreasing the survival in patients, and narrowing potential treatment options (Gatenby). An assortment of chemotherapeutic drugs and dosing schedules were tested on ER+ endocrine-resistant MCF7 breast cancer cells in an immunodeficient mouse model. After the cessation of treatment, some mouse models’ tumors remained stable or began to shrink. Several immunodeficient mouse models have indicated unexpectedly high levels of neutrophils stemming from an unknown origin. We aim to understand if neutrophils' innate immunity may affect tumor size post-chemotherapy treatment and if it has therapeutic implications along with adaptive therapy. MCF7 breast cancer tumors were extracted from the mice, embedded in wax, and sliced, and immunofluorescence was performed to detect neutrophils and nuclear components. Currently, the protocol is in its third round of optimization.
ContributorsMestas, Lauren (Author) / Maley, Carlo (Thesis director) / Richker, Harley (Committee member) / Marquez Alcaraz, Gissel (Committee member) / Barrett, The Honors College (Contributor) / School of Life Sciences (Contributor)
Created2024-05
Description
Tissue regeneration is a complex process that activates both developmental and metabolic signaling pathways (Kashio & Miura, 2020). The wing imaginal disc in Drosophila melanogaster has been invaluable in discerning what pathways are activated during tissue regeneration, which is typically done by genetically or physically wounding the wing disc and using fluorescent markers to track different signals. However, despite its importance in other regeneration contexts (Tafesh-Edwards & Eleftherianos, 2020), immune signaling has not been well studied in this tissue. Furthermore, what we do know about tissue regeneration and immune signaling is specific to apoptotic cellular death, less is known about other types of cellular death, such as necrotic cellular death and the consequent signaling systems that result from necrosis. Drosophila have an open immune system and only possess innate immunity (Pastor-Pareja et al., 2008), making them an ideal model to study hemocyte involvement in tissue regeneration. Hemocytes are equivalent to blood cells in vertebrates, and are involved in immunological response (Kurucz et al., 2003). In this work, we observed hemocyte accumulation during injury-induced regeneration. Cellular damage was induced using a genetic ablation system known as DUAL Control, with hemipterous CA and GluR1 used to induce apoptotic and necrotic cell death respectfully. We have discovered that while hemocytes are recruited to the wing disc upon both apoptotic and necrotic injury, necrotic tissue has more hemocytes adhered than apoptotic tissue. The difference in adherence could be due to basement membrane integrity being damaged more severely in necrotic discs than apoptotic discs. Our results show that hemocytes are attracted to wing discs that have undergone necrotic damage, indicating that the immune system plays some sort of role in necrotic cellular death. Though the immune response to different types of tissue damage in Drosophila is much simpler than in vertebrate models, there are many similarities between the two, and could lead to research involving human immune signaling as it pertains to regeneration.
ContributorsZustra, Ayla (Author) / Harris, Robin (Thesis director) / Gile, Gillian (Committee member) / Barrett, The Honors College (Contributor) / School of Life Sciences (Contributor)
Created2022-05
Description
The study of broad therapeutic advantages of dance is a growing field of interdisciplinary study. Yet, direct health benefits of dance from a molecular standpoint are still largely unknown. Literature review of dance performance displays in birds as well as other creatures and use of creative tools to analyze the diverse, lifelong experiences of dancers helped shed some light on the subject. Although dance experience exposes harms tied to the social constraints of how the form is experiences buried under joyful takeaways of dance, research supports overall health benefits from moderate amounts of dance maintained in perfect equilibrium.
ContributorsWilliams, Caroline (Author) / Fitzgerald, Mary (Thesis director) / Moore, Marianne (Committee member) / Barrett, The Honors College (Contributor) / School of Life Sciences (Contributor) / School of Music, Dance and Theatre (Contributor)
Created2022-05
P2RX7 promotes a pro-memory signature in effector CD8+ T cells dependent on Zeb2 negative regulation
Description
Memory CD8+ T cells protect against secondary viral infections. They develop and maintain exclusively in circulation (e.g. central memory - Tcm) or are excluded from re-circulation (resident memory - Trm). The extracellular ATP receptor P2RX7 promotes both Tcm and Trm generation. High (P2RX7hi) P2RX7-expressing early effector cells show survival, memory and pluripotency genes. Conversely, many terminal effector (TE) and apoptosis genes are upregulated in low (P2RX7lo) P2RX7-expressing cells. Among these genes is the zinc-finger transcriptional repressor Zeb2, which promotes TE differentiation at the expense of the memory cell pool. Given that Zeb2 was higher in P2RX7lo early effector cells, we postulated that Zeb2 ablation would allow P2RX7-deficient CD8+ T cells to skew towards memory subsets. To test this, we used RNP-based CRISPR-Cas9 to knockout Zeb2 in wild type or P2RX7-deficient P14 cells. At the memory timepoint, Zeb2 ablation led to a rescue of the ability of P2RX7-deficient cells to differentiate into the CD62L+ Tcm and CD69hiCD103hi Trm subsets, as well as increase the population of each. Our data suggest that P2RX7 imprints a pro-memory signature that is, to some extent, dependent on the negative regulation of Zeb2.
ContributorsVan Dijk, Sarah (Author) / Holechek, Susan (Thesis director) / Borges da Silvs, Henrique (Committee member) / Barrett, The Honors College (Contributor) / School of Life Sciences (Contributor) / School of Molecular Sciences (Contributor) / School of International Letters and Cultures (Contributor)
Created2021-12
Description
Purinergic receptors play an important role in the response to infectious diseases by sensing damage-associated molecular patterns (DAMPs). The P2X family of purinergic receptors is known to recognize extracellular ATP (eATP) at different affinities. One of these receptors, P2X3, shows high affinity for eATP, but its role in modulating responses to infectious diseases has not been studied. Using the pulmonary infection model with influenza virus PR8 strain on wild type (WT) and P2RX3-deficient (P2RX3-KO) mice, we aimed to discover the role of P2RX3 in influenza infection in the lungs. We found that there was not a significant difference in the severity of disease in WT and P2RX3-KO mice during the acute phase, but there was more fibrotic tissue visible in P2RX3-KO mice lungs on day 40 post infection (p.i.) using Masson’s trichrome staining. To further investigate these differences, we analyzed myeloid cell populations and flu-specific lymphocytes in the infected lungs. We found that there was a significant decrease in the number of antigen-specific CD4+ T cells in the lungs of P2RX3-KO mice after 7 days p.i. After performing t-SNE (t-distributed stochastic neighbor embedding) analysis on CD4+ T cells of P2RX3-KO and WT mice, we discovered that P2RX3-KO mice had a population of cells which was not present in the WT mice. This population showed high expression of most proteins such as T-bet and BCL6, which is not characteristic of the typical Th1 population induced by influenza virus. Using in vitro activation and differentiation of Th1 CD4+ T cells from WT and P2RX3-KO mice, we found that P2RX3-KO CD4+ T cells had greater expression of markers related to Tfh (T follicular helper cells), such as ICOS and CXCR5, and overall hyperactivation, demonstrating irregular Th1 differentiation. Taken together, these results suggest that P2RX3 may be linked to the maintenance of “healthy” CD4+ T cells and may be important in preventing fibrosis in influenza infection.
ContributorsWhite, Emily (Author) / Florsheim, Esther (Thesis director) / Borges da Silva, Henrique (Committee member) / Barrett, The Honors College (Contributor) / Department of Psychology (Contributor) / School of Life Sciences (Contributor)
Created2024-05