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:

"Estrogen receptor α, or ERα, is believed to play a central role in controlling inflammation. Research suggests that ERα does that by regulating anti-inflammatory signaling in the microglia, the only immune cells that reside in the brain. Now, a new study confirms ERα’s beneficial role in the brains of mice. The work explored one mechanism believed to prime ERα to fight inflammation, the attachment of a phosphoryl group to a specific amino acid in ERα’s structure -- a process known as “phosphorylation”. To test that mechanism, researchers blocked the phosphorylation of ERα in microglia from mice. That absence, it turned out, compromised the cells’ defenses against inflammation – leaving mice vulnerable to negative effects. For example, some mice with blocked ERα phosphorylation were obese and showed weakened motor skills. Further study could help explain how phosphorylated ERα regulates brain immunity and inflammation in brain 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:

"Inflammatory bowel diseases (IBDs), such as Crohn’s disease and ulcerative colitis, affect more than 0.3% of the Western population. The sheer complexity of these diseases presents a major challenge to treatment, as it has created a disconnect between microbiologists studying the effects of the microbiome, immunologists studying immune responses, and clinicians who treat individuals with IBD. To mount a more holistic approach, researchers recently examined the crosstalk between immune cells and bacteria in the colon. Experiments revealed the significance of bacterial products called outer membrane vesicles, or OMVs. OMVs are tiny sacs of cellular material released by bacteria as a way of communicating with immune cells. In patients with Crohn’s disease or ulcerative colitis, OMVs elicited only a small fraction of their normal immune response, suggesting a breakdown in immune–microbiota communication..."

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:

"Alpha-1 antitrypsin deficiency (AATD)-mediated liver disease is a form of toxic inflammation associated with the retention of mutant alpha-1 antitrypsin within cells. Patients with this disease typically show fibrosis and cirrhosis of the liver. Unfortunately, the mechanism of AATD-mediated liver disease is not well understood. To gain some insight, researchers recently explored the role of extracellular vesicles in the progression of AATD-mediated liver disease. They isolated vesicles from the plasma of individuals with both AATD and liver disease and compared them with vesicles from healthy individuals in terms of cytokine and chemokine expression as well as miRNA expression. Vesicles from individuals with AATD were shown to activate hepatic stellate cells in vitro, which is believed to be one of the first steps of fibrosis. a process mediated by the NF-κB and JAK/STAT 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:

"Cirrhosis is a chronic disease involving permanent scarring of the liver And it's currently the 11th leading cause of death worldwide In its most advanced form, the disease impairs kidney function, causing what’s known as hepatorenal syndrome While inflammation is believed to play a role in cirrhosis No studies have examined the link between inflammation and hepatorenal syndrome until now Researchers from Spain tracked inflammation responses in 161 patients hospitalized for advanced cirrhosis Patients who developed hepatorenal syndrome showed a much stronger inflammatory response than those without the disease The relatively small patient sample means that these results should be interpreted with caution But the findings could still provide meaningful clues for treating patients with cirrhosis Helping doctors identify potential targets for slowing disease progression Solé et al..."

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:

"Despite a large reduction in AIDS-related deaths as a result of HIV antiretroviral programs, the global incidence of HIV has only decreased by 16% in the past 10 years. One hotspot is in South Africa, where young women in particular face high rates of HIV infection. In a recent study, researchers followed up on their previous observation that female genital tract (FGT) inflammation increases HIV risk by evaluating the relationship between FGT inflammation and microbial function in 113 young South African women at high risk of HIV infection. Using metaproteomics to characterize a total of 3,186 microbial and human proteins from vaginal wall swabs, they found that women with elevated FGT inflammation had increased non-optimal bacteria and decreased lactobacilli. Reduced cell wall organization and peptidoglycan biosynthesis were also associated with high FGT inflammation levels..."

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 blood–retinal barrier is a collection of tightly packed cells that keeps harmful substances from entering the retina. These cells include retinal microvascular endothelial cells, RMECs. RMEC dysfunction contributes to certain inflammatory eye diseases, including diabetic retinopathy, uveitis, and age-related macular degeneration. A recent study examined the effects of one emerging cause of this dysfunction: the leakage of mitochondrial DNA into the cytosol. Pathological stimuli, including hydrogen peroxide (H2O2), high glucose (HG), and liposaccharide (LPS), caused mitochondrial DNA to leak out of RMECs from rats through a process known as mitochondrial permeability transition pore opening. Leaked mitochondrial DNA regulated the expression of the signaling molecule cGAS. In turn, cGAS stimulated the expression of the pro-inflammatory molecules CCL4, CXCL10, and IFNB1 and transcription factor IRF1..."

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:

"Dysregulation of the IL-6-induced JAK/STAT cascade is associated with severe inflammatory and proliferative diseases. The cascade is normally tightly controlled by proteins such as the feedback inhibitor SOCS3 and the tyrosine phosphatase SHP2. SOCS3 increases the stability of late IL-6-induced STAT3 activation across cells with different STAT3 levels and reduces the signal magnitude. but whether SHP2 similarly affects robustness and information transfer remains unclear. Researchers recently used multiplexed single-cell analyses and information theory approaches to clarify SHP2’s roles. They found that SHP2 improved the robustness of STAT3 activation under basal conditions (in the absence of the cytokine IL-6) and during early IL-6 signalling levelling the degree of activation across cells with heterogeneous expression levels of STAT3. However, it did not affect the robustness of late IL-6-induced STAT3 activation..."

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:

"Meniscal tears are one of the most frequent knee injuries and the most common pathology leading to arthroscopic surgery in the United States. It’s no surprise, then, that there’s been a lot of research into how repairing these injuries affects joint kinematics and biomechanics. But meniscal injury also causes changes on the microscopic scale, in the joint microenvironment. Tracking these changes could provide important clues into the cellular processes that promote the development of conditions like post-traumatic osteoarthritis. Researchers from the NYU Langone Orthopedic Center are using synovial fluid biomarkers to take a closer look at this link. The team evaluated 41 patients undergoing arthroscopic surgery to treat a symptomatic, unilateral meniscal injury. Synovial fluid samples were collected at the time of surgery from both the operative and contralateral knee. The concentrations of 10 synovial fluid biomarkers were then compared between knees..."

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

In our resource, we highlight the role of the viral non-structural proteins and their role in blocking host interferon signaling of the innate immune system.  In addition, we also describe the host immune response specifically the cytokine signaling clouds in the variation in severity of patients living with COVID-19.  Finally, we apply these latest peer-reviewed research on host immune response to SARS-CoV-2 in the context of integrated immunology framework linked with three-dimensional learning in life science education and topics on social justice dimensions of vaccination access in global health.  Through the social justice lens and global health perspectives, we provide an innovative framework to engage undergraduates in the field of integrated immunology and developmental biology in both remote and hybrid-flexible (HyFlex) learning settings.

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:

"Tumor cells create an environment that fosters growth by communicating with surrounding tumor and non-tumor cells. Understanding and ultimately disrupting this communication is the goal of many emerging anticancer strategies. A recent study recently examined how the oncogene YAP orchestrates cellular communication during the formation of liver tumors. Researchers identified several secreted factors that are induced by YAP to adjust cell-cell communication in support of tumor growth. One of these, a protein known as PAI-1, regulates the expression of factors associated with cellular senescence and was found to be linked to poor clinical outcomes in patients with liver cancer. Experiments showed that YAP, with the help of a separate protein (TEAD4), controls PAI-1 expression and secretion ultimately generating a tumor-supportive microenvironment..."

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:

"Colorectal cancer is among the top three most lethal types of cancer worldwide, and its incidence is increasing. If colorectal cancer spreads to bone, the balance between the natural breakdown of old bone tissue and the production of new bone can be severely disrupted, leading to fractures, excess calcium in the blood, and other issues. Understanding the processes driving colorectal cancer bone metastasis can therefore guide the development of new treatments to combat these disorders. To meet this need, researchers recently evaluated the effects of CCL7, a small protein involved in immunity, which is also thought to have an important role in cancer progression and metastasis. They found increased production of CCL7 in the bone marrow of mice with colorectal cancer bone metastasis, but the injection of a CCL7-neutralizing antibody prevented a reduction in bone volume. The team also showed that CCL7 stimulated the movement of osteoclast precursors, cells that are involved in breaking down bone tissue..."

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:

"Inflammation in the brain is a hallmark of many neurodegenerative diseases, including Alzheimer’s and Huntington’s disease. One of the key orchestrators of neuroinflammation is IL-6, a cytokine secreted by brain-resident cells called astrocytes. While low levels of IL-6 support neurons and synapses in the brain higher levels of IL-6 are produced in response to injury or infection, triggering a series of proinflammatory signaling cascades. Unfortunately, how astrocytes regulate IL-6 expression remains unclear. A recent study evaluated signaling pathways involved in IL-6 gene regulation, including β-catenin, TCFs/LEF, C/EBP, and NF-κB. Using human astrocytes, researchers silenced or overexpressed the signaling proteins and measured IL-6 levels. They found that TCF/LEF induces IL-6 in the presence of ATF2, while β-catenin inhibits IL-6 by interacting with TCF/LEF. Interestingly, neither of these signaling pathways is known to regulate IL-6 in other cell types..."

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