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BIO15 Exam5 Chapter 16: Introduction to the Immune System Overview of the Immune System (Part 1/3) For ease of study, the immune system is divided into branches—but just keep in mind that the immune system is actually extremely complex, and we could spend an entire year just covering its mechanisms. So there's a lot of information in these next few chapters. You're going to want to spend a fair amount of time understanding how the immune system functions and how it interacts with different components to protect us from these microbe infections. Innate vs. Acquired Immune Defenses Chapter 16 covers the portions of the immune system that you're born with—this is called the innate immune system. Later on, we'll talk about the acquired immune defense , which is covered in Chapter 17 and includes B cells and T cells. The innate immune system is further broken down into: First line of defense Second line of defense First Line of Defense: Physical, Chemical, and Genetic Barriers Physical Barriers Skin : Coats the entire body and serves as a physical barrier. Microbes cannot get across intact skin. Some microbes have enzymes that can break down skin, but for the most part, if it's intact, it's your primary protection. Mucous membranes : Trap microbes to prevent them from entering deeper into the respiratory or digestive tracts. Ciliary escalator : Cilia lining the trachea trap inhaled microbes. When you cough, cilia push the microbes out—like an escalator. Lacrimal apparatus : Duct in the eye that releases fluids to wash out microbes. Saliva : Helps wash microbes from the mouth. Urine : Flows outward, flushing out pathogens from the urinary tract. Vaginal secretions : Flow outward to prevent microbes from entering further. Endothelia (blood-brain barrier) : Most microbes cannot cross it. Those that can may cause diseases like encephalitis or meningitis—more on these in the disease chapters. Normal flora : The mere presence of non-pathogenic microbes on your body helps by competitive exclusion of pathogens. Taking probiotics helps maintain healthy flora. Chemical Barriers Sebaceous glands : Release chemicals that alter the skin’s pH, making it inhospitable for many pathogens. Lysozyme : Found in sweat, tears, and tissues. It’s an enzyme that cleaves the glycosidic bond in peptidoglycan cell walls—destroying bacteria. Gastric juice : Its acidity inhibits the majority of pathogens. Antimicrobial peptides : These proteins break down various microbes. Second Line of Defense: Cellular and Soluble Factors Before diving into the cellular mechanisms, let’s briefly review blood composition :
Blood = plasma + formed elements o Plasma : Liquid portion containing proteins, gases, vitamins, hormones, electrolytes, etc. o Formed elements : Include red blood cells (RBCs), white blood cells (WBCs), and platelets. RBCs : Transport oxygen and CO₂; not discussed much here. Platelets : Involved in clotting; also not a focus here. White Blood Cells : Primary focus for this chapter. White Blood Cells (WBCs): Categories and Development White blood cells are relatively low in concentration but play a crucial role. When you draw a WBC count from a patient with an infection, their levels can indicate the nature of the infection—whether it’s bacterial, viral, or even eukaryotic. WBCs include: Neutrophils Eosinophils Basophils Monocytes (→ macrophages) Lymphocytes (→ B cells and T cells) Dendritic cells Mast cells Natural killer cells Origin and Differentiation All WBCs originate from stem cells in the bone marrow , which differentiate into various lineages depending on gene expression and signals. You are constantly building these stem cells, which further divide into: Monoblasts → Monocytes → Macrophages Lymphoblasts → B cells, T cells Erythroblasts → Red blood cells This isn't something to memorize, but it's important to understand that differentiation determines the cell type and function in your immune response. Self vs. Non-Self Recognition A fundamental property of the immune system is recognizing self vs. non-self. Your immune system must: Recognize your own cells and not attack them. Recognize foreign cells and attack them. Two major features allow this:
Not true granulocytes or agranulocytes. Found in the skin and tissues—main barrier areas. Have large nuclei and can phagocytose. Secrete cytokines to signal immune response. Key in early detection and antigen presentation (more in Chapter 17). Example: Can recognize an HIV-infected self-cell and trigger an immune response. Natural Killer (NK) Cells Agranulocytes. Present throughout the body. Kill virus-infected or cancerous self-cells non-specifically. Help shut down virus replication early. Lymphocytes (Overview) We'll study these in detail in Chapter 17: B cells T cells These are involved in specific (acquired) immune responses. Lymphatic System Parallels the blood system, spreads throughout the body. Lymph nodes filter lymph and indicate infection if inflamed. o Bacterial infections : more likely to cause lymph node inflammation. o Viral infections : less inflammation typically. Lymph is similar to blood except it lacks red blood cells. ========== Chapter 16 Part 2: Innate Immune System Mechanisms (Part 2/3) ========== There are six primary mechanisms that function in the innate immune system that you need to understand:
- Inflammation
- Phagocytosis
- Fever
- Complement
- Chemical Mediators
- Natural Killer Cells We're going to go through each one, starting with inflammation. 1. Inflammation
Inflammation is a response to trauma , and it can be caused by several things: Mechanical injury (e.g., breaking a bone) Chemical exposure Infection by a pathogen For this class, we’re going to focus on the mechanism of inflammation caused by a pathogen , but overall, the mechanism is fairly similar regardless of the cause. Purpose of Inflammation: Mobilizes and attracts more immune system cells to the site of infection Aids in tissue repair Localizes and removes harmful substances to prevent spread Destroys microbes Clinical Signs of Inflammation: There are four primary signs: Redness Heat Swelling Pain Each of these has Latin names that you'll learn in nursing or PT school, but for now, just remember the four basic signs. Mechanism of Inflammation: Let’s say someone gets stabbed by a dirty knife. The knife breaks the first line of defense (the skin), and bacteria are introduced into the dermis. Macrophages and neutrophils in the area recognize the bacteria. These cells release cytokines (e.g., histamine, kinins, prostaglandins, leukotrienes). Cytokines activate other immune processes. What cytokines do: Cause vasodilation , which brings more blood and immune cells to the site. Promote margination and diapedesis (white blood cells leaving blood vessels and entering tissues). This is what’s shown in the diagram (and the YouTube video on Canvas — highly recommended). It shows how epithelial cells change gene expression during inflammation and begin producing a receptor called selectin that helps white blood cells bind and pass through the lining. As cytokine concentration increases: White blood cells are pulled into the tissue. Once the bacteria is removed, cytokines stop being produced. Margination and diapedesis stop. The tissue repairs itself.
Contents are released into the extracellular space. However, some specific proteins from the bacteria are retained and displayed on the MHC (major histocompatibility complex). This is important in activating the acquired immune system (Chapter 17). Here's another diagram version of this process: Shows PAMP receptors on the phagocyte and PAMPs on the bacterial cell. Once bound, the same sequence of engulfment, fusion with lysosome, degradation, and presentation occurs.
3. Chemical Mediators These are chemicals released by immune cells to communicate with each other. Types of Chemical Mediators: Cytokines : Already discussed — they trigger inflammation and communication between cells. Vasoactive mediators : Cause changes in blood vessels (either dilation or constriction). Chemokines : Stimulate movement of white blood cells. o Selectins are a type of chemokine. ========== Chapter 16 Part 3: Innate Immune System Mechanisms (Part 3/3) ========== Fever (briefly mentioned): Often in healthcare, they’ll have you treat the fever. (No mechanism detail provided here—focus shifts immediately to the next topic.) 1. Interferon There are many antimicrobial proteins produced by the body, but the one we’re going to focus on here is interferon. There are many different types of interferon. Your body produces different types depending on the virus or trigger involved. We even use interferon as a drug treatment sometimes. For this class, we’re not going to focus on the different types—just the general mechanism. General Function: Interferon is a protein produced by your body in response to: Viral infections Microbial infections RNA immune products Antigens For this lecture, we're only focusing on interferon produced in response to a viral infection. Mechanism Overview: Think back to when we talked about viral replication in animal viruses: The virus enters the host cell via endocytosis or fusion.
The capsid disassembles in the cytoplasm. The virus starts taking over the host cell’s machinery to replicate. Meanwhile: The infection triggers transcription and translation of interferon protein. This happens even while the virus is replicating. The cell that’s already infected can’t save itself , but it releases interferon into the environment. Interferon’s Action on Neighboring Cells:
- Released interferon travels to neighboring cells.
- Interferon binds to receptors on the plasma membrane of neighboring cells.
- Interferon does not enter the neighboring cell.
- Instead, it activates a signaling cascade , which causes gene expression changes.
- These genes produce antiviral proteins. Result: When viruses try to infect these neighboring cells: o The antiviral proteins already present attack the viral nucleic acid. o This deactivates the virus and stops replication. Other Roles of Interferon: Protects neighboring cells Activates T-cells and B-cells Activates natural killer (NK) cells Inhibits cancer cells Activates macrophages Enhances phagocyte action 🔹 **Short-term interferon release is beneficial.
- Complement System** The complement system involves over 26 different blood proteins that: Constantly circulate in the blood Are normally inactive Are activated under certain conditions Types of Activation (3 total): For this class, you only need to remember the classical activation. Key Concepts: Complement system is non-specific — not tailored to a specific pathogen.
Attract more immune cells like macrophages and neutrophils 🔹 There’s a video on Canvas that explains the complement cascade—make sure to watch it. 🔹 You should be able to draw this cascade and explain the steps for the exam.
3. Natural Killer (NK) Cells NK cells are not phagocytic. They respond to any microbe generically. Key Activation Trigger: NK cells look for missing or altered MHC (major histocompatibility complex) markers. MHC = “self” marker on your cells. If the MHC is missing or abnormal , the NK cell is activated. Actions of NK Cells: 1. Release perforins : o These drill holes in the target cell’s membrane. 2. Release granzymes : o Enter through those holes and trigger apoptosis (programmed cell death). Targets of NK Cells: Virus-infected cells Cancer cells Any abnormal or infected host cells NK Cells also release: Interferon : o Stimulates cells to produce antiviral proteins o Helps protect the cell from further viral infection The remaining slides in your presentation are diagrams with text removed. These are intended to review and self-study. 🔹 By exam time, you should be able to explain these mechanisms in your own words and draw the processes.
