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:

"Many patients undergoing chemotherapy for cancer develop a serious side effect called chemotherapy-induced peripheral neuropathy (CIPN). CIPN involves pain, tingling, burning, or numbness in the hands and feet and is caused by neuroinflammation triggered by the protein HMGB1, but the exact mechanisms aren’t clear. To learn more and help find a treatment, researchers recently examined the plasma of human patients and mice with oxaliplatin-induced CIPN. They found that the levels of HMGB1 and its target enzyme MMP-9 (a pain marker) were elevated in CIPN plasma and that a higher dose of oxaliplatin was associated with higher HMGB1 levels and worse pain. In cell experiments, HMGB1 was degraded—and inflammatory molecule expression was suppressed—when the enzyme AMPK was activated suggesting that AMPK activation might be beneficial for CIPN. These effects were dependent on the protein SR-A1..."

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

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:

"CCL2 is a small cell-signaling protein that recruits immune cells to sites of inflammation. CCR2 is CCL2’s receptor. Together, CCL2 and CCR2 create an inflammatory and immune-suppressive microenvironment, which promotes tumor growth and progression and induces resistance to anticancer drugs. A recent review highlights research on the therapeutic potential of targeting this so-called “CCL2-CCR axis”. Circulating levels of CCL2 are particularly elevated in individuals with obesity. Studies on men with prostate cancer suggest that inhibiting CCL2 signaling can significantly inhibit tumor growth and invasion. More work is needed to differentiate natural CCL2 levels in patients from tumor-derived CCL2 involved in the formation and spread of tumors, which could lead to new ways of attacking cancer and cancer resistance..."

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 immunosuppressive tumor microenvironment (TME) plays essential roles in cancer development and progression. Exosomes mediate crosstalk between tumor cells and other stromal or immune cells in the TME, but how tumor-derived exosomes promote the progression of bladder cancer, one of the most common types of cancer, remains unclear. To find out, researchers recently examined the effects of exosomes extracted from the conditioned medium (CM) of MB49 bladder cancer cells. The researchers found that the cancer-derived exosomes were ingested by mouse macrophages both in vitro and in vivo and that they induced macrophage polarization toward the immunosuppressive M2 phenotype. Exosome-secreting MB49 cells induced tumor growth in mice, but the exosome inhibitor GW4869 reduced tumor growth, macrophage M2 polarization and immunosuppression, confirming the pro-tumor effects of the cancer-derived exosomes..."

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:

"Membrane-enclosed extracellular vesicles, exosomes, are a critical part of intercellular communication in many biological systems. However, the regulation and biological implications of exosome excretion and uptake remain unclear. A recent study examined the role of cellular retinoic acid (RA) binding protein (Crabp1) in exosome secretion and its relationship to receptor interacting protein 140 (RIP140), a pro-inflammatory transcription co-regulator. Crabp1 knockout mice consistently showed deficits in negative control of exosome secretion and exhibited increased vulnerability to systemic inflammation. Crabp1 knockout mice had significantly elevated RIP140-containing exosomes in their blood and cerebrospinal fluid. Cell culture experiments suggested that exosome secretion can transfer RIP140 from neurons to macrophages, where it promotes macrophage inflammatory polarization..."

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:

"Endoplasmic reticulum (ER) stress in tumor cells caused by protein misfolding can promote cancer progression. It does this by enabling immune escape and by upregulating PD-L1, a protein that activates protumor immune cells called M2 macrophages. This process may involve small extracellular vesicles known as exosomes, but the mechanisms are unclear. A new study investigated these mechanisms in oral squamous cell carcinoma (OSCC), the most common head/neck cancer. The ER stress markers PERK, ATF6, and GRP78 were upregulated in OSCC tissues from patients and were related to poor overall survival. In addition, the levels of the ER stress proteins were positively associated with PD-L1 expression and macrophage infiltration in tumor tissues. Exosomes derived from an ER-stressed OSCC cell line in vitro (Exo-ERs)contained more PD-L1 than control exosomes (Exo-Cons), and the Exo-ERs upregulated PD-L1 in macrophages and polarized macrophages toward the protumor M2 type both in vitro and in vivo..."

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:

"Pain is useful. It’s a natural mechanism for protecting the body in humans and other animals. However, pain that is chronic and persists longer than it should is considered a disease. Research has revealed that pain is often the result of an important interplay between the immune system and the nervous system. When the body produces an inflammatory response to injury, or disease, inflammation can activate [pain circuits], sensitize them, and lead to increased and ongoing pain. Now, using nanosized particles of medicine that momentarily switch inflammation off, researchers have discovered new clues as to how chronic pain unfolds and how it might be relieved. The team began by inducing immune-based chronic pain in rats. They did so surgically by constricting the right sciatic nerve with loosely tied sutures, causing swelling and inflammation through the infiltration of white blood cells, immune cells including monocytes that become macrophages..."

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:

"Heart attacks are dangerous events that lead to a massive loss of heart cells, called cardiomyocytes. The catastrophic damage can be treated by generating cardiomyocytes from stem cells and transplanting them into the heart. The stem cells can then proliferate in the space before becoming new cardiomyocytes by differentiating and maturing. But little is known about how macrophages from the injury site impact stem cell-derived cardiomyocytes. To learn more, researchers cultured these stem cells, called induced pluripotent stem cells (iPSCs), with macrophages of several subtypes. Macrophages start in a non-polarized phenotype (M0) and then can polarize between pro-inflammatory (M1) and anti-inflammatory (M2) phenotypes. The pro-inflammatory M1 phenotype macrophages were likely to be found at the injury site, and they inhibited iPSC differentiation and maturation..."

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:

"Researchers from Australia have uncovered a unique way that drug-resistant breast cancer cells trick the immune system, potentially allowing them to spread through the body unchecked. The mechanism relies on cancer cells’ shedding of microparticles, tiny sacs filled with protein and nucleic acids, from their membranes. It’s been shown that these sacs bind with other cells to transfer drug resistance, but now it’s clear that they also use the particles to shut down the immune system. To find out what causes this inhibition, the researchers focused on white blood cells known as macrophages. These cells are found throughout the body and mainly work to destroy pathogens and other harmful cells by engulfing them. But this key defense mechanism fails as breast cancer progresses. Because microparticles help cancer cells spread harmful traits to recipient cells, the researchers thought these particles might also play a role in immune evasion..."

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:

"New research suggests that cells from the umbilical cord can be programmed to gobble up and kill disease-causing bacteria. When deployed in rats, such cells could effectively reduce signs of acute lung injury, pointing to an alternative route for fighting lung disease in humans. These are mesenchymal stromal cells. Their chameleon-like ability to form into bone, cartilage, or fat in the body has made them valuable for tissue repair and regeneration. But recent studies have shown that these cells can also help boost the immune system. They do this by releasing bioactive pockets of cellular matter that are believed to signal immune cells like macrophages to action. In rats with bacterial lung disease, that ability appears to provide significant relief. Researchers found that injecting mesenchymal cells from human umbilical cords could reduce signs of pneumonia caused by E. coli and increase animal survival. What’s more, they could actually enhance that effect..."

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:

"Atherosclerosis is a chronic inflammatory process where lipids accumulate along the arterial wall. One key protein in atherosclerosis development is AIBP (Apolipoprotein A-I binding protein). AIBP exists both inside and outside cells, but only secreted AIBP is well characterized in atherosclerosis. A recent study found that AIBP is highly expressed in human and mouse atherosclerotic lesions and that the AIBP was concentrated within the inner membrane of macrophage mitochondria. Macrophages are immune cells that can have pro- or anti-inflammatory phenotypes. The interplay between these phenotypes plays a pathogenic role in atherosclerosis. In this study, blocking the production of AIBP in bone marrow aggravated atherosclerosis and increased macrophage infiltration in a mouse model. This bone-marrow-specific AIBP deficiency increased the cleavage of the protein PINK1 (PTEN-induced putative kinase 1)..."

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