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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:

"For the first time, scientists have figured out how to grow and extend the life of primary airway epithelial cells from newborns and young children. These cells line our nasal passages and lungs, protecting us from pathogens, and controlling our immune responses to allergens. Differences in these cells may help explain why certain infants develop wheezing and asthma later in life, but studying them has been challenging because they are difficult to obtain in babies and usually die in culture after dividing a few times. Now, researchers at Children’s National Medical Center in Washington, D.C. and George Washington University have devised a way to reprogram pediatric airway epithelial cells so that they survive, creating a new model to study respiratory disorders that take hold early in life. The team collected airway epithelial cells from 23 donors, including newborns, infants and young children..."

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:

"Liver ischemia and reperfusion injury (IRI) is a major cause of liver transplant failure. Such injuries involve many inflammatory processes and activate liver macrophages. Activation of the Notch1 protein and the Notch pathway modulate inflammatory responses, but the exact molecular mechanisms at play are not yet understood. To narrow this gap, a recent study investigated macrophage Notch1 in a mouse model of liver IRI. Liver ischemia and reperfusion activated the Notch1 protein in liver macrophages, and knocking out the Notch1 gene from macrophage precursors worsened the damage and increased inflammation. Macrophage Notch1 deficiency also inhibited the expression of β-catenin. This led to a TAK1-mediated inflammatory response and RIK3-mediated hepatocyte necroptosis, a type of inflammatory cell rupture. Restoring Notch1 to macrophages using lentivirus alleviated the liver damage in this knockout model and reduced some of the inflammatory response..."

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:

"Viruses must adapt to the microenvironments of their hosts’ cells in order to establish infection often “hijacking” the machinery of host cells to serve their own purposes. Many types of mammalian host cells release exosomes (small vesicles containing various molecules) to communicate with neighboring cells. but how viruses exploit exosomes remains unclear. To learn more, researchers recently screened Epstein–Barr virus (EBV) proteins in exosomes that might promote infection. They identified the protein BGLF2, which normally exists in the viral tegument, through several screening strategies. Tegument proteins are typically released from viruses after they enter the host cell cytoplasm to mediate infectivity, supporting an infection-driving role of exosomal BGLF2. Additional in vitro experiments revealed that BGLF2-containing exosomes enhanced viral gene expression and suppressed host innate immunity..."

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:

"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.

Pathogens can invade the body if a breach occurs in the barriers formed by the skin and mucus membranes, for example a wound, they must be detected and destroyed by cellular and humoral means. The cells involved in the cellular response to a wound are mast cells, macrophages, granulocytes, and monocytes.

The innate response to bacterial infection lies in its first-response role of detection of a foreign organism. By using the tools of Pattern-Recognition Receptors (PRRs), the innate response flags up problems while the adaptive response gets itself organized.

Because viruses invade host cells to take over a host's cellular machinery, the innate system has a more difficult time detecting viruses as foreign agents. However, there is a give-away element of the viral attack that the innate system can recognize: the double-stranded RNA (dsRNA) produced by a virus in its replication phase. Because mammalian cells only ever produce single-stranded RNA, the presence of dsRNA signals a foreign intruder. dsRNA can be detected by TLR-3R on the cell surface or intracellularly by the presence of dsRNA-dependent protein kinase.

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:

"Sometimes viruses release RNA into the host’s cytosol, and detecting that RNA is a critical part of the host’s antiviral immune response. But cells need to have a set of brakes to regulate these responses, otherwise they can trigger harmful overproduction of type I interferon proteins. The kinase MST4 is one part of this ‘braking’ system. Previous work found that MST4 limits damaging inflammatory responses by adding a phosphate group to the adaptor protein TRAF6. But researchers wanted to know how MST4 might regulate type I interferon production. So, in a recent study, they determined that MST4 also competes with another TRAF protein, TRAF3, to bind MAVS. MAVS is a key antiviral signaling protein, and when MST4 binds it instead of TRAF3, type I interferon production is slowed. They also found that MST4 facilitated interactions between MAVS and the ubiquitin ligase Smurf1, which encouraged degradation of MAVS..."

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 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:

"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:

"Myocardial infarction (MI), also known as a heart attack, is a common but serious cardiac emergency. The severity and mortality of MI are related to overactivation of immune cells called neutrophils. Specifically, excessive activation of a process called neutrophil degranulation appears to impair MI recovery. During degranulation, molecules that can help fight pathogens and repair tissue damage are released from cytoplasmic granules. This is normally beneficial, but too much degranulation can aggravate MI-related injury. Four main types of granules are released: primary/azurophilic, secondary/specific, tertiary/gelatinase, and secretory granules. These granule types are synthesized and released at different times and contain different mixtures of molecules. For example, primary granules contain the enzyme MPO, excess levels of which can impair ventricular healing and function after MI, while secondary granules contain NGAL, which can increase the risk of plaque formation and promote inflammation and fibrosis..."

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