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The Immune System: Innate and Adaptive Body Defenses: Part A

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The Immune System: Innate and Adaptive Body Defenses: Part A 10/9/2014 PowerPoint® Lecture Slides Immunity prepared by Barbara Heard, Atlantic Cape Community • Resistance to disease College • Immune system – Two intrinsic systems C H A P T E R 21 • Innate (nonspecific) defense system • Adaptive (specific) defense system The Immune System: Innate and Adaptive Body © Annie Leibovitz/Contact Press Images © 2013 Pearson Education, Inc. Defenses: © 2013 Pearson Education, Inc. Part A Immune System Immunity • Functional system rather than organ • Innate defense system has two lines of system defense • Innate and adaptive defenses intertwined – First - external body membranes (skin and • Release and recognize many of same mucosae) defensive molecules – Second - antimicrobial proteins, phagocytes, • Innate defenses do have specific and other cells pathways for certain substances • Inhibit spread of invaders • Innate responses release proteins that • Inflammation most important mechanism alert cells of adaptive system to foreign molecules © 2013 Pearson Education, Inc. © 2013 Pearson Education, Inc. Immunity Figure 21.1 Overview of innate and adaptive defenses. Surface barriers • Skin • Mucous membranes • Adaptive defense system Innate – Third line of defense attacks particular foreign defenses Internal defenses • Phagocytes substances • Natural killer cells • Inflammation • Takes longer to react than innate system • Antimicrobial proteins • Fever Humoral immunity • B cells Adaptive defenses Cellular immunity • T cells © 2013 Pearson Education, Inc. © 2013 Pearson Education, Inc. 1 10/9/2014 Innate Defenses Surface Barriers • Surface barriers ward off invading • Protective chemicals inhibit or destroy pathogens microorganisms – Acidity of skin and secretions – acid mantle – – Skin, mucous membranes, and their inhibits growth secretions – Enzymes - lysozyme of saliva, respiratory • Physical barrier to most microorganisms mucus, and lacrimal fluid – kill many • Keratin resistant to weak acids and bases, microorganisms bacterial enzymes, and toxins – Defensins – antimicrobial peptides – inhibit • Mucosae provide similar mechanical barriers growth – Other chemicals - lipids in sebum, dermcidin in sweat – toxic © 2013 Pearson Education, Inc. © 2013 Pearson Education, Inc. Surface Barriers Internal Defenses: Cells and Chemicals • Respiratory system modifications • Necessary if microorganisms invade – Mucus-coated hairs in nose deeper tissues – Cilia of upper respiratory tract sweep dust- – Phagocytes and bacteria-laden mucus toward mouth – Natural killer (NK) cells • Surface barriers breached by nicks or cuts – Antimicrobial proteins (interferons and - second line of defense must protect complement proteins) deeper tissues – Fever – Inflammatory response (macrophages, mast cells, WBCs, and inflammatory chemicals) © 2013 Pearson Education, Inc. © 2013 Pearson Education, Inc. Phagocytes Mechanism of Phagocytosis • Neutrophils most abundant but die fighting • Phagocyte must adhere to particle – Become phagocytic on exposure to infectious – Some microorganisms evade adherence with material capsule • Macrophages develop from monocytes – chief • Opsonization marks pathogens—coating by phagocytic cells – robust cells complement proteins or antibodies • Free macrophages wander through tissue spaces, • Cytoplasmic extensions bind to and engulf e.g., alveolar macrophages • Fixed macrophages permanent residents of some particle in vesicle called phagosome organs; e.g., stellate macrophages (liver) and • Phagosome fuses with lysosome microglia (brain) phagolysosome © 2013 Pearson Education, Inc. © 2013 Pearson Education, Inc. 2 10/9/2014 Figure 21.2a Phagocytosis. Figure 21.2b Phagocytosis. Slide 1 1 Phagocyte Innate defenses Internal defenses adheres to pathogens or debris. 2 Phagocyte forms pseudopods that Phagosome eventually engulf the (phagocytic particles, forming a vesicle) phagosome. Lysosome 3 Lysosome fuses with the phagocytic vesicle, forming a phagolysosome. Acid hydrolase enzymes 4 Lysosomal enzymes digest the particles, leaving a residual body. 5 Exocytosis of the A macrophage (purple) uses its cytoplasmic vesicle removes extensions to pull rod-shaped bacteria indigestible and (green) toward it. Scanning electron residual material. micrograph (4800x). Events of phagocytosis. © 2013 Pearson Education, Inc. © 2013 Pearson Education, Inc. Mechanism of Phagocytosis Natural Killer (NK) Cells • Pathogens killed by acidifying and digesting with • Nonphagocytic large granular lymphocytes lysosomal enzymes • Attack cells that lack "self" cell-surface • Helper T cells cause release of enzymes of receptors respiratory burst, which kill pathogens resistant to lysosomal enzymes by – Induce apoptosis in cancer cells and virus- infected cells – Releasing cell-killing free radicals – Producing oxidizing chemicals (e.g., H2O2) • Secrete potent chemicals that enhance – Increasing pH and osmolarity of phagolysosome inflammatory response • Defensins (in neutrophils) pierce membrane © 2013 Pearson Education, Inc. © 2013 Pearson Education, Inc. Inflammatory Response Inflammatory Response • Triggered whenever body tissues injured • Cardinal signs of acute inflammation: • Prevents spread of damaging agents 1. Redness • Disposes of cell debris and pathogens 2. Heat • Alerts adaptive immune system 3. Swelling 4. Pain • Sets the stage for repair (Sometimes 5. Impairment of function) © 2013 Pearson Education, Inc. © 2013 Pearson Education, Inc. 3 10/9/2014 Inflammatory Response Inflammatory Response • Begins with chemicals released into ECF • Inflammatory mediators by injured tissues, immune cells, blood – Kinins, prostaglandins (PGs), and proteins complement • Macrophages and epithelial cells of • Dilate local arterioles (hyperemia) boundary tissues bear Toll-like receptors – Causes redness and heat of inflamed region (TLRs) • Make capillaries leaky • 11 types of TLRs recognize specific • Many attract leukocytes to area classes of infecting microbes • Some have inflammatory roles • Activated TLRs trigger release of cytokines that promote inflammation © 2013 Pearson Education, Inc. © 2013 Pearson Education, Inc. Inflammatory Response: Edema Inflammatory Response • Capillary permeability exudate to • Clotting factors form fibrin mesh tissues – Scaffold for repair – Fluid containing clotting factors and – Isolates injured area so invaders cannot antibodies spread – Causes local swelling (edema) – Swelling pushes on nerve endings pain • Pain also from bacterial toxins, prostaglandins, and kinins – Moves foreign material into lymphatic vessels – Delivers clotting proteins and complement © 2013 Pearson Education, Inc. © 2013 Pearson Education, Inc. Figure 21.3 Inflammation: flowchart of events. Innate defenses Internal defenses Phagocyte Mobilization Initial stimulus Physiological response Signs of inflammation Tissue injury Result • Neutrophils lead; macrophages follow Release of inflammatory chemicals Release of leukocytosis- (histamine, complement, inducing factor kinins, prostaglandins, etc.) – As attack continues, monocytes arrive Leukocytosis (increased numbers of white • 12 hours after leaving bloodstream blood cells in bloodstream) Arterioles Increased capillary Attract neutrophils, macrophages dilate permeability monocytes, and lymphocytes to Leukocytes migrate to area (chemotaxis) injured area • These "late-arrivers" replace dying neutrophils and Local hyperemia Capillaries (increased blood leak fluid Margination remain for clean up prior to repair flow to area) (exudate formation) (leukocytes cling to capillary walls) Diapedesis • If inflammation due to pathogens, Leaked protein-rich Leaked clotting (leukocytes pass through fluid in tissue spaces proteins form interstitial capillary walls) clots that wall off area to prevent injury to complement activated; adaptive immunity surrounding tissue Phagocytosis of pathogens Heat Redness Pain Swelling and dead tissue cells (by neutrophils, short-term; by macrophages, long-term) elements arrive Locally increased Possible temporary Temporary fibrin Pus may form temperature increases impairment of patch forms metabolic rate of cells function scaffolding for repair Area cleared of debris Healing © 2013 Pearson Education, Inc. © 2013 Pearson Education, Inc. 4 10/9/2014 Figure 21.4 Phagocyte mobilization. Slide 1 Phagocyte Mobilization Innate defenses Internal defenses • Steps for phagocyte mobilization 1. Leukocytosis: release of neutrophils from bone marrow in response to leukocytosis- Inflammatory inducing factors from injured cells chemicals diffusing 4 Chemotaxis. 2. Margination: neutrophils cling to walls of from the Neutrophils follow inflamed chemical trail. capillaries in inflamed area in response to site act as CAMs chemotactic Capillary wall agents. Basement 3. Diapedesis of neutrophils membrane Endothelium 4. Chemotaxis: inflammatory chemicals (chemotactic agent) promote positive chemotaxis of neutrophils 1 Leukocytosis. 2 Margination. 3 Diapedesis. Neutrophils enter Neutrophils cling Neutrophils flatten blood from bone to capillary wall. and squeeze out of marrow. capillaries. © 2013 Pearson Education, Inc. © 2013 Pearson Education, Inc. Antimicrobial Proteins Interferons • Include interferons and complement • Family of immune modulating proteins proteins – Have slightly different physiological effects • Some attack microorganisms directly • Viral-infected cells secrete IFNs (e.g., IFN • Some hinder microorganisms' ability to alpha and beta) to "warn" neighboring reproduce cells – IFNs enter neighboring cells produce proteins that block viral reproduction
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