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:

"Acute myeloid leukemia (AML) is a type of blood and bone marrow cancer with a low survival rate. One reason AML is so deadly is because it can evade the immune system, in part by downregulating proteins like MICA, which normally marks damaged or cancerous cells in the body for immune destruction. To improve treatment prospects, researchers recently searched for molecules that can restore MICA levels in AML cells. They found that the transcription factor KFL4 is involved in MICA expression. In addition, treating cultured AML cells with the KLF4-activating compound APTO253 successfully induced MICA expression, while inhibiting the expression of the cancer gene MYC. These changes made the AML cells more susceptible to being killed by immune cells. Although studies in animals and humans are still needed, these findings reveal that APTO253 can improve immune cells’ ability to detect and kill AML cells and suggest that targeting KFL4/MICA is a promising option for AML treatment..."

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:

"Renal cancer affects over 400,000 people each year, and new treatment options are needed. A new study unraveled a paradox taking place in the immune systems of cancer patients. Myeloid-derived suppressor cells (MDSCs), driven by tumor cells, have the ability to suppress the immune responses of T cells, preventing T-cell recognition of tumor cells and allowing immune escape. However, mice and humans with renal tumors do not experience systemic immunosuppression. Researchers used mice to examine renal cancer-derived exosomes (RDEs), extracellular vesicles derived from tumor cells. They found that the proportion and activity of MDSCs in the spleen and bone marrow changed after internalization of RDEs. RDE-stimulated MDSCs inhibited T cell proliferation and cytotoxicity, and these effects were antigen-specific and driven by the molecule HSP70 in RDEs and TLR2 on MDSCs, explaining the targeted immunosuppression of the renal cancer-specific immune response..."

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

Biology is designed for multi-semester biology courses for science majors. It is grounded on an evolutionary basis and includes exciting features that highlight careers in the biological sciences and everyday applications of the concepts at hand. To meet the needs of today’s instructors and students, some content has been strategically condensed while maintaining the overall scope and coverage of traditional texts for this course. Instructors can customize the book, adapting it to the approach that works best in their classroom. Biology also includes an innovative art program that incorporates critical thinking and clicker questions to help students understand—and apply—key concepts.

By the end of this section, you will be able to:Describe physical and chemical immune barriersExplain immediate and induced innate immune responsesDiscuss natural killer cellsDescribe major histocompatibility class I moleculesSummarize how the proteins in a complement system function to destroy extracellular pathogens

By the end of this section, you will be able to:Describe how signaling pathways direct protein expression, cellular metabolism, and cell growthIdentify the function of PKC in signal transduction pathwaysRecognize the role of apoptosis in the development and maintenance of a healthy organism

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 ligand protein PD-L1 on tumor cells can bind to the receptor protein PD-1 on T cells. This binding negatively regulates T cells to suppress immunity, facilitating large-scale tumor growth. Antibody drugs have been designed to block cell-surface PD-L1/PD-1 binding, but they’re not very effective, possibly because tumor cells can secrete extracellular vesicles (EVs) that express PD-L1. The PD-L1 on EVs can also induce immunosuppression, leading to drug resistance. EV PD-L1 plays tumor-promoting roles in many cancers, such as breast cancer, prostate cancer, and melanoma, and unlike cell-surface PD-L1, which isn’t expressed stably enough to be reliable, EV PD-L1 may be a useful biomarker. Because of its location, EV PD-L1 may also be a good treatment target. For example, drugs preventing EV release have been shown to activate antitumor responses in melanoma cells and to reduce prostate tumor growth and increase anti-PD-L1 efficacy against colon cancer in mice..."

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:

"Livestock health is critical to food security, and parasite infections are a major threat. Gastrointestinal helminths have a huge impact on health and welfare of livestock and on food production worldwide. Resistance to parasiticides has become widespread, making the control of these infections highly challenging. Control strategies thus far have targeted either the parasite or the host’s immune response, but a third party may hold the key to addressing this issue. Microbes residing within the livestock gut are likely to contribute to the immunopathology of helminth infections. A recent study examined the relationships between gastrointestinal helminths, the host immune system, and the gut microbiota. Using DNA sequencing and confocal microscopy, researchers assessed fluctuations in the microbiota and local immune responses of vaccinated and unvaccinated helminth-infected sheep. Their results showed that gut microbial composition changed significantly during parasite infection..."

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:

"Residing in the stomachs of over half the human population, the bacterium Helicobacter pylori, also known as H pylori, has become a major cause of digestive complications, ranging from peptic ulcers to stomach cancer. But despite this link, scientists still aren’t sure how these disorders arise after infection. Now, researchers have homed in on a single protein produced by H pylori that seems to rev up the immune system, causing a state of inflammation that may pave the way for cancer growth or other types of gut breakdown. The protein, HP1454, is naturally released from H pylori -- both actively by living cells and passively as cells die. The scientists found that when special immune cells known as T cells encounter this secreted HP1454, they kick into action, mounting an inflammatory response. This relationship was particularly strong in people with stomach cancer..."

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:

"Autoimmune disease happens when the body’s immune system reacts to its own cells and tissues. Central to this process are regulatory T cells (Tregs), which control the inflammatory CD4 T cell response. Understanding how to boost Tregs will help researchers develop new therapies for autoimmunity. In a recent study, researchers zeroed in on a broad regulator of cell differentiation, migration, and proliferation – MKL-1. Using molecular techniques, they examined its interaction with STAT5, a transcriptional activator central to Treg development. After overexpressing or silencing MKL-1 and STAT5 in cell lines, they evaluated protein interactions and Treg gene expression. The results showed that MKL-1 acts a coactivator for STAT5b targets in Tregs. MKL-1 was upregulated during Treg differentiation, and overexpressing MKL-1 enhanced the expression of Treg markers. Silencing STAT5b blocked MKL-1 from activating Treg genes, showing its dependence on STAT5b for its function..."

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:

"In endocytosis, the cell plasma membrane folds inward and pinches off to form intracellular vesicles. Originally, endocytosis was thought to primarily facilitate feeding and pathogen neutralization, but it is now known to regulate numerous processes in eukaryotic cells, such as signaling, membrane composition, mitosis, movement, and morphogenesis. Endocytosis also plays many roles in T cells through both clathrin-dependent and clathrin-independent mechanisms. For example, clathrin-mediated endocytosis regulates the receptors on the plasma membrane and internalizes α/β-type T cell antigen receptors (TCRs). Through clathrin-independent pathways, endocytosis internalizes TCRζ and the IL-2Rβ complex and recycles TCRαβ. Clathrin-independent endocytosis also helps T cells bind to antigen-presenting cells of the immune system and ingest pathogens and other foreign materials to aid in host defense and immune surveillance..."

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:

"A major turning point for tumor immunotherapy was the discovery of immune checkpoint proteins, which suppress immunity to facilitate tumor growth. The discovery prompted the development of immune checkpoint inhibitors (ICIs) that can help fight even metastatic and chemoresistant cancers. ICIs that target the proteins CTLA-4, PD-1, and PD-L1 are particularly promising for cancer treatment. These drugs can be used either alone or with other therapies to enhance treatment efficacy. For example, they can be combined with traditional chemotherapy, radiotherapy, antiangiogenic therapy, and cancer vaccines to improve outcomes. In addition, combinations of CTLA-4- and PD-1-blocking ICIs can be used to treat cancers like melanoma. However, despite the encouraging results in some studies, many patients fail to respond to ICIs. ICIs can also exert various immune-related adverse effects on the skin, colon, liver, lungs, kidneys, and heart, and some tumors can become resistant to the drugs..."

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:

"The COVID-19 outbreak is a devastating ongoing pandemic. Most patients experience mild symptoms, but some develop severe disease. An even smaller subset of patients develop acute respiratory distress syndrome, which has high mortality. To unravel the molecular mechanisms at play, researchers retroactively examined clinical records from patients with confirmed COVID-19. They found that severe cases had increased levels of inflammatory damage markers and lower T cell numbers – including total T cells, CD4+, and CD8+ T cells – than moderate cases. Analysis of public single-cell RNA-seq data revealed severe cases had increased clonal expansion of macrophages and highlighted that high-TREM2-expressing macrophages were dramatically enriched in moderate cases of COVID-19. Cell communication analysis suggested that high-TREM2 macrophages drive ligand-receptor cross talk, which may contribute to the exhaustion of CD8+ 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:

"PD-L1 is a powerful cloaking protein for cancer cells. Abundant PD-L1 on their surface binds with the receptor PD-1 on immune cells. The PD-L1/PD-1 axis transfers inhibitory signaling to the immune system that the cancer cells pose no danger. How this cloaking process unfolds has remained unclear. Now, researchers report the prominence of the enzyme USP22. USP22 is overexpressed in malignant tumors of several types, including those of the lung. Initial experiments on human lung cancer cells showed that USP22 might regulate PD-L1. A closer look revealed that USP22 deubiquitinated and stabilized PD-L1. USP22 enlists the help another protein, CSN5, to stabilize PD-L1. By inhibiting USP22 genetically, researchers could suppress the formation of tumors. Targeting USP22 in the clinic could therefore be one way to decloak cancer cells and make them vulnerable to existing anti-cancer therapies..."

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 tyrosine kinase p56 Lck is critical for T-cell development and activation. Lck initiates signaling events downstream of the T-cell receptor (TCR) by phosphorylating ITAM motifs located within CD3 chains, which in turn recruits the kinase Zap-70 to the activated TCR/CD3 complex. But while the regulation of its enzymatic activity is mostly attributed to two tyrosine residues, Y394 and Y505, Lck has an additional highly conserved tyrosine, Y192, whose function in the regulation of Lck activity is not fully understood. A recent study examined the role of this residue in primary T cells and T cell lines. Using knock-in mice expressing a phosphomimetic mutant of Lck (LckY192E), researchers found that Lck Y192E bound poorly to CD45 and showed hyperphosphorylation at Y505, similar to previous data in Jurkat cell lines. However, in vitro, Lck Y192E had normal enzymatic activity in both human and mouse T cells, suggesting that this residue acts independently of the interaction with CD45..."

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.