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:Explain adaptive immunityCompare and contrast adaptive and innate immunityDescribe cell-mediated immune response and humoral immune responseDescribe immune tolerance

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:

"Helicobacter pylori is one of the most prevalent human pathogens worldwide, with over 4 billion people infected. Without antibiotics, the bacteria can persist in the GI tract of its host for life and cause gastritis, ulcers, and even gastric cancer. Although H. pylori induces a severe inflammatory response, it can’t be cleared by its host’s immune system. A recent study sought an explanation for why the immune response against H. pylori is not effective. Researchers examined the characteristics of human monocyte-derived DCs infected with H. pylori. They found that H. pylori-infected DCs had higher levels of a suppressor of cytokine signaling (SOCS) protein. SOCS3 expression was specifically increased by H. pylori infection. This change was mediated by a pathway relying on the type IV secretion system, TNFα, and p38. Silencing SOCS3 in DCs prior to infection resulted in increased cytokine signaling and downregulated T cell activation and proliferation..."

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:

"Autophagy is a catabolic process in which intracellular components are degraded in lysosomes. Stresses such as nutrient deficiency, hypoxia, and chemotherapy can trigger autophagy, making autophagy relevant to cancer treatment. Autophagy appears to play complex dual roles in cancer immune escape. For example, autophagic degradation of the immune checkpoint protein PD-L1 generally enhances T cell activation and suppresses tumor growth, but cancer cells can encapsulate PD-L1 and another checkpoint protein, CD47, in endosomes to prevent their degradation. In addition, MHC-I/II autophagy enables cancer cell immune escape and inhibits antigen presentation and T cell activation. However, autophagic mitochondrial degradation, termed mitophagy, can improve the antitumor immune response. Therefore, autophagy can positively or negatively affect cancer immune escape, which may depend on the experimental context, and autophagy may synergize with immune cells to regulate cancer immune surveillance..."

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