This resource is a video abstract of a research paper created by Research Square on behalf of its authors. It provides a synopsis that's easy to understand, and can be used to introduce the topics it covers to students, researchers, and the general public. The video's transcript is also provided in full, with a portion provided below for preview:

"An effective, tightly regulated immune response is critical for patients to recover from viral infections like COVID-19. Understanding immune regulation can allow researchers to develop better therapeutics and management techniques for patients. One class of factors involved with immune regulation are soluble immune mediators, which play roles in the dynamic interactions between ligands and membrane-bound receptors. Normally, soluble immune mediators help maintain and restore health after pathological events, but sometimes their dysregulation causes pathology instead. SARS-CoV-2 infection impacts many of these soluble immune mediators and, through them, many physiological processes. Thus, dysregulated shifts in the concentration of some of these molecules could be playing a significant role in COVID-19 severity and mortality..."

The rest of the transcript, along with a link to the research itself, is available on the resource itself.

This resource is a video abstract of a research paper created by Research Square on behalf of its authors. It provides a synopsis that's easy to understand, and can be used to introduce the topics it covers to students, researchers, and the general public. The video's transcript is also provided in full, with a portion provided below for preview:

"The “universal adaptor” protein MyD88 orchestrates innate immunity by propagating signals from receptor proteins called TLRs and IL-1Rs.Specifically, activation of these receptors enables MyD88-dependent formation of an organizing center known as the myddosome. An alternate form of MyD88 lacking the intermediate domain (ID), MyD88S, can silence the immune response, but the mechanism isn’t well understood. To learn more, researchers recently investigated the functions of MyD88 variants and mutants in cells and with computer programs. They found that the variant MyD88S is recruited to the newly forming myddosome, where it inhibits further myddosome maturation by preventing incorporation of additional components. In normal MyD88, the ID doesn’t have a well-defined secondary structure, but the amino acid tyrosine at site 116 is required for myddosome formation and related signaling..."

The rest of the transcript, along with a link to the research itself, is available on the resource itself.

This resource is a video abstract of a research paper created by Research Square on behalf of its authors. It provides a synopsis that's easy to understand, and can be used to introduce the topics it covers to students, researchers, and the general public. The video's transcript is also provided in full, with a portion provided below for preview:

"The concept of trained immunity suggests that exposure to nonpathogenic microbes or their metabolites can enhance an organism’s immune response later in life. But while trained immunity has been addressed by many studies focusing on vertebrate animals, little is known about its role in invertebrates. A recent study showed that microorganism exposure early in development increased the survival of the Pacific oyster when challenged with infectious disease. Researchers cultured Pacific oysters in filtered and UV-treated seawater that had either been enriched with naturally occurring microbes or unmanipulated as a control. These oysters and their offspring were then exposed to the virus that causes Pacific oyster mortality syndrome, a disease that devastates oyster farms worldwide. The team found increased survival not only among the oysters directly exposed to the microbe-enriched seawater but also among their progeny..."

The rest of the transcript, along with a link to the research itself, is available on the resource itself.

This resource is a video abstract of a research paper created by Research Square on behalf of its authors. It provides a synopsis that's easy to understand, and can be used to introduce the topics it covers to students, researchers, and the general public. The video's transcript is also provided in full, with a portion provided below for preview:

"Dental caries are the most common health condition worldwide and can progress to pulpitis, a painful dental pulp infection. Odontoblasts at the pulp-dentin interface fight against these conditions by preventing bacterial invasion. In other pathological conditions, mitochondrial DNA (mtDNA)-related cell stress activates the cGAS-STING pathway, which contributes to inflammation, but whether mtDNA and cGAS-STING signaling are involved in caries- and pulpitis-associated odontoblast inflammation is unknown. A recent study used molecular techniques to investigate this possibility in patient tissues and an odontoblast-like cell line. cGAS and STING levels were elevated in human caries and pulpitis tissues, and the levels increased as inflammation worsened. In the cell line, the inflammation-inducing bacterial product liposaccharide (LPS) increased the expression of cGAS-STING pathway proteins, suggesting pathway activation, but silencing STING diminished some inflammation-related changes..."

The rest of the transcript, along with a link to the research itself, is available on the resource itself.

This resource is a video abstract of a research paper created by Research Square on behalf of its authors. It provides a synopsis that's easy to understand, and can be used to introduce the topics it covers to students, researchers, and the general public. The video's transcript is also provided in full, with a portion provided below for preview:

"N6-methyl-adenosine (m⁶A) methylation is the most abundant epigenetic modification on mRNA and lncRNA. This modification is regulated by m⁶A writers, readers, and erasers, and its proper regulation is critical for innate and adaptive immunity, especially since m⁶A can play different roles depending on the transcript region, cell type, or specific regulators involved. For example, in the innate immune system, m⁶A can promote the antitumor and antiviral activity of NK cells. It can also activate disease- fighting M1 macrophages, reduce inflammation, and encourage dendritic cell maturation and activity. On the other hand, m⁶A can prevent dendritic cells from cross-presenting tumor antigens to prime T cells, hindering the antitumor response. In the adaptive immune system, m⁶A promotes T cell homeostasis but also suppresses T follicular helper cell development and it can either exacerbate or inhibit HIV-1 infection in CD4⁺ T cells..."

The rest of the transcript, along with a link to the research itself, is available on the resource itself.

This resource is a video abstract of a research paper created by Research Square on behalf of its authors. It provides a synopsis that's easy to understand, and can be used to introduce the topics it covers to students, researchers, and the general public. The video's transcript is also provided in full, with a portion provided below for preview:

"Could doctors one day prescribe electrical stimulation to fight a bacterial infection? Work by an interdisciplinary team of researchers at AIMES suggests that might be possible. In line with the Goals of the United Nations’ 2030 Agenda, researchers at AIMES are dedicated to promoting “Good Health and Well-Being” by achieving a better understanding of bacterial infections and the body’s defenses against them. Some of their latest findings reveal a new aspect of host–pathogen interactions. In addition to the cascade of chemical signals that are activated when bacteria invade, the body might also conduct electrical signals across nerves—enabling the infected organ to call distant parts of the body to action. The team uncovered this form of “biological telecommunication” by studying rats with kidney infections caused by strains of E. coli. Within as little as 4 hours of infection, they could detect an immune response all the way in the spleen..."

The rest of the transcript, along with a link to the research itself, is available on the resource itself.

This lesson plan is designed to help students review their knowledge of the human immune system through an interactive game called, Defend Your Body. Students will explore instances in which the body's immune system may malfunction. The first part of the lesson will review the main functions of the human immune system through a game called Defend Your Body. After playing the game, students will engage in a class discussion about the similarities of the gameplay and the function of a real immune system. During the second part of the lesson, students will revisit the game, to recognize instances where the human immune system may deviate from its normal functions. Students will then research various diseases that affect the immune system and create a new variation of Defend Your Body that simulates the effects of the disease.

This resource is a video abstract of a research paper created by Research Square on behalf of its authors. It provides a synopsis that's easy to understand, and can be used to introduce the topics it covers to students, researchers, and the general public. The video's transcript is also provided in full, with a portion provided below for preview:

"Regulatory T cells (Tregs) normally maintain balance in the immune system, but Treg dysfunction can lead to inflammation and immune disorders. The protein PPARγ enhances Treg generation and function, so it’s a promising therapeutic target for these conditions. However, the mechanisms of PPARγ’s effects on Tregs are unclear. To learn more, researchers recently tested the effects of several PPARγ-activating drugs on Tregs derived from mouse lymph node cells. The activators increased Treg production and the expression of immunosuppressive molecules important for Treg function. They also enhanced Tregs’ energy supply by upregulating CD36 and CPT1, two proteins involved in fatty acid oxidation (FAO). Furthermore, PPARγ activation increased N-linked glycosylation, a process that links carbohydrate molecules to proteins and thereby altered the cell-surface abundance of the receptors TβRII and IL-2Rα, affecting the TGF-β/Smad and IL-2/STAT5 signaling pathways..."

The rest of the transcript, along with a link to the research itself, is available on the resource itself.

This resource is a video abstract of a research paper created by Research Square on behalf of its authors. It provides a synopsis that's easy to understand, and can be used to introduce the topics it covers to students, researchers, and the general public. The video's transcript is also provided in full, with a portion provided below for preview:

"The activation of toll-like receptors (TLRs) is critical to detecting potentially harmful microbes, but overactivation can be life-threatening, leading to autoimmune and inflammatory diseases. While much research has been dedicated to positive regulators of TLR signaling, such as protein serine/threonine kinases, much less has focused on phosphatases, which counterbalance and limit TLR signaling. Fortunately, a growing number of studies are exploring the roles of these enzymes and how they might be harnessed to prevent excessive immune activation. Two important families of protein phosphatases are phospho-protein phosphatases (PPPs) and metal-dependent protein phosphatases (PPMs). PPPs contain a highly conserved catalytic core domain, which can combine with regulatory subunits to home in on specific enzymatic targets. PPMs, on the other hand, rely on magnesium or manganese ions and do not form multi-subunit complexes..."

The rest of the transcript, along with a link to the research itself, is available on the resource itself.

This resource is a video abstract of a research paper created by Research Square on behalf of its authors. It provides a synopsis that's easy to understand, and can be used to introduce the topics it covers to students, researchers, and the general public. The video's transcript is also provided in full, with a portion provided below for preview:

"The COVID-19 pandemic, caused by the virus SARS-CoV-2, has spread rapidly since 2019. COVID-19 symptoms are mild in some patients but severe and even life-threatening in others and there are still no reliable treatments for severe COVID-19. In a recent study, researchers investigated the factors related to COVID-19 severity in hospitalized patients with mild or severe illness. Specifically, they investigated the patients’ immune characteristics and signaling pathways involving immune proteins called IFN-Is. Compared with healthy controls, patients with COVID-19 had lower counts of many types of immune cells but higher counts of Th17 cells in their blood and the differences were more drastic in patients with severe disease. In addition, individuals with severe COVID-19 had much lower levels of IFN-I signaling molecules than healthy controls..."

The rest of the transcript, along with a link to the research itself, is available on the resource itself.

This resource is a video abstract of a research paper created by Research Square on behalf of its authors. It provides a synopsis that's easy to understand, and can be used to introduce the topics it covers to students, researchers, and the general public. The video's transcript is also provided in full, with a portion provided below for preview:

"Low-molecular-weight carrageenan (Cg) is a seaweed-derived sulfated polysaccharide that has been widely used to stimulate inflammation in preclinical studies. However, exactly how Cg induces inflammation is still unclear. Using cell culture and mouse model experiments, investigators examined the molecular basis of two inflammatory processes triggered by Cg: macrophage activation and cytokine production. Mouse peritoneal macrophage primary cell cultures were stimulated with a form of Cg, κ-Cg. The researchers found that κ-Cg activates peritoneal macrophages to produce pro-inflammatory cytokines such as TNF and IL-1β. While κ-Cg-induced TNF production and secretion depend on TLR4/MyD88 signaling, the production of pro-IL-1β relies on the TLR4/TRIF/SYK/ reactive oxygen species signaling pathway..."

The rest of the transcript, along with a link to the research itself, is available on the resource itself.

This resource is a video abstract of a research paper created by Research Square on behalf of its authors. It provides a synopsis that's easy to understand, and can be used to introduce the topics it covers to students, researchers, and the general public. The video's transcript is also provided in full, with a portion provided below for preview:

"Lymphotoxin β receptor (LTβR) is a key regulator of the immune response. Its signaling cascades control the development and maintenance of secondary lymphoid organs and immune cell development. Although many aspects of its signaling have been characterized, one important aspect remains unclear. After ligand binding, LTβR is internalized via endocytosis – but the precise mechanisms involved have not yet been characterized. A recent study investigated the contribution of LTβR internalization to its signaling potential. Researchers found LTβR localized to endocytic vesicles and the Golgi apparatus. After ligand binding, LTβR was trafficked via endosomes to lysosomes for degradation, downregulating signaling. Multiple entry pathways – clathrin-mediated, dynamin-dependent, and clathrin-independent – were used for receptor internalization, and without clathrin and dynamin, cells had elevated signaling through the NF-κB pathway..."

The rest of the transcript, along with a link to the research itself, is available on the resource itself.

This resource is a video abstract of a research paper created by Research Square on behalf of its authors. It provides a synopsis that's easy to understand, and can be used to introduce the topics it covers to students, researchers, and the general public. The video's transcript is also provided in full, with a portion provided below for preview:

"Mitochondrial stress is a key trigger of innate immune responses. Sources of stress include environmental changes, genetic mutations, and pathogenic infection. Mitochondria respond by releasing mitochondrial DAMPs and cytochrome c into the cytosol that induce inflammation and apoptosis through activating inflammasomes, cGAS and apoptotic caspases. One way cells manage mitochondrial stress is by eliminating dysfunctional mitochondria, a process known as “mitophagy.” Mitophagy regulatory pathways are classified as ubiquitin (Ub)-dependent or Ub-independent (receptor-dependent). Growing evidence shows that mitophagy can be induced by certain bacteria and viruses. Co-opting the mitophagy process enables these pathogens to evade hosts’ immune defense. Much remains to be learned about the mechanisms that pathogens employ to hijack host mitophagy. Understanding these mechanisms could point to new therapeutic strategies for fighting infection and related diseases..."

The rest of the transcript, along with a link to the research itself, is available on the resource itself.

This resource is a video abstract of a research paper created by Research Square on behalf of its authors. It provides a synopsis that's easy to understand, and can be used to introduce the topics it covers to students, researchers, and the general public. The video's transcript is also provided in full, with a portion provided below for preview:

"Phosphorylated STAT1 (P-STAT1) is an important mediator of interferon-induced antiviral immunity. During interferon signaling, P-STAT1 dimerizes and accumulates in the nucleus with the help of the protein importin to affect gene transcription and elicit immune responses. In a positive feedback loop, P-STAT1 also induces further STAT1 expression, thereby increasing the cytoplasmic levels of unphosphorylated STAT1 (U-STAT1), a protein that regulates apoptotic cell death. However, the impact of U-STAT1 on the P-STAT1-mediated immune response is unclear. To learn more, researchers recently cotransfected cells with wild-type P-STAT1 and a permanently unphosphorylated U-STAT1 mimic. Interestingly, the U-STAT1 mimic prevented nuclear accumulation of P-STAT1 during interferon gamma (IFNγ) stimulation, but it didn’t impair downstream P-STAT1 signaling, indicating that some P-STAT1 could still enter the nucleus to exert its effects..."

The rest of the transcript, along with a link to the research itself, is available on the resource itself.

This resource is a video abstract of a research paper created by Research Square on behalf of its authors. It provides a synopsis that's easy to understand, and can be used to introduce the topics it covers to students, researchers, and the general public. The video's transcript is also provided in full, with a portion provided below for preview:

"T cell receptor (TCR) signaling helps initiate appropriate T cell responses during immune reactions. Protein kinase D isoforms are suggested to be part of the TCR signaling pathway, but PKD3's role isn't clear. To learn more, researchers recently examined PKD3 in cultured mouse T cells. Upon T cell activation, both PKD3 and PKD2 (a better-characterized PKD) were downregulated. In mice, PKD3 deletion enhanced the adaptive immune response to immunization with ovalbumin/alum. Specifically, PKD3-knockout mice had heavier spleens and more splenic T follicular helper cells than wild-type (wt) mice. In addition, ex vivo activated T helper cells from PKD3-deficient mice produced more IL-2 (and IFN-γ) than those from wt mice, indicating hyperresponsiveness and implying that PKD3 normally limits the immune response. In contrast, PKD3 expression didn’t affect the differentiation or activation of naïve mouse T helper cells in vitro..."

The rest of the transcript, along with a link to the research itself, is available on the resource itself.

This resource is a video abstract of a research paper created by Research Square on behalf of its authors. It provides a synopsis that's easy to understand, and can be used to introduce the topics it covers to students, researchers, and the general public. The video's transcript is also provided in full, with a portion provided below for preview:

"Chronic rhinosinusitis is one of the most common diseases among humans, affecting approximately 12% of the adult population globally. It is characterized by inflammation of the nasal cavity and sinuses, causing facial pressure and pain as well as long-term loss of smell. Benign masses called nasal polyps can also develop and cause chronic nasal obstruction, but the exact cause of this disease is unknown. Recent research has indicated that toxins produced by the bacterium _Staphylococcus aureus_, particularly enterotoxin B (SEB), may play an important role. SEB is thought to stimulate the immune system by activating proteins such as toll-like receptor 2 and pro-inflammatory cytokines and by causing reactive oxygen species production and endoplasmic reticulum stress. This inflammatory response may then disrupt the integrity of the epithelial cells in the nose and sinuses..."

The rest of the transcript, along with a link to the research itself, is available on the resource itself.

This resource is a video abstract of a research paper created by Research Square on behalf of its authors. It provides a synopsis that's easy to understand, and can be used to introduce the topics it covers to students, researchers, and the general public. The video's transcript is also provided in full, with a portion provided below for preview:

"The Chinese tongue sole (Cynoglossus semilaevis) is a popular and economically important farmed flatfish. But this species is susceptible to outbreaks of vibriosis, a bacterial infection that can cause significant losses. The intestinal microbiome in many animals can impact disease resistance, but little is known about its role in fish diseases. So, researchers used families of C. semilaevis selectively bred to be either vibriosis-resistant or susceptible. The gene expression of the fish, as well as the microbial community structure and functional capabilities, were different between the two families. There was also evidence that the intestinal microbiome was influencing the expression of immune-related genes in the fish. Specifically, the vibriosis-resistant fish had gene expression changes that would reduce inflammation and balance the immune response..."

The rest of the transcript, along with a link to the research itself, is available on the resource itself.