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BLG 10A/B (51)

Immune System

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Emily Agard

BLG10B ­ Immune System 1. Innate system (nonspecific) - prepared, responds within minutes. 2nd line of defense gets called when 1st line has been penetrated, and it relies on internal defenses (antimicrobial proteins, phagocytes & other cells) 2. Adaptive (specific) defense system - attacks particular foreign substances (3rd line) Innate Defenses • Mechanical barriers that cover body surfaces & cells/chemicals • Reduce workload of adaptive system by preventing entry/spread of MO Surface Barriers - Skin & Mucosae • First line of defense - highly effective • Skin & mucous membranes produce a variety of protective chemicals • Respiratory tract mucosa have structural modifications (tiny mucus coated hairs, cilia) Internal Innate Defenses: Cells & Chemicals Phagocytes • Neutrophils become phagocytic on encountering infectious material in tissues • Macrophages derive from monocytes • Free macrophages wander throughout tissues searching for foreign invaders • Fixed macrophages (stellate macrophages in liver) are permanent residents of their organ Phagocytosis • Engulfs particulate matter • Cytoplasmic extensions bind to particle & pull it inside, enclosing it in a vesicle • Resting phagosome then fuses with a lysosome to form a phagolysosome • In order for a phagocyte to ingest pathogen, it must adhere to pathogen • Many bacteria have external capsules that cover this coat & our immune system bypasses this issue by coating pathogens with opsonins • Opsonins = proteins/Ab+ that make handles that phagocyte receptors bind (opsonization) • Neutrophils & macrophages can acidify the phagolysosome, digesting its contents but some pathogens (Tb) can multiply within the phagolysosome • In this case, T helper cells release chemicals that stimulate the macrophage, activating additional enzymes producing a respiratory burst o Liberates highly destructive free radicals o Produces oxidizing chemicals o Increases phagolysosome's pH & osmolarity (activates other enzymes) • Neutrophils also pierce pathogen's membrane using defensins - antimicrobial proteins • When phagocytes can't ingest, they can release toxic chemicals into extracellular fluid Natural Killer (NK) Cells • Can lyse & kill cancer cells/virus infected cells before adaptive immune system • Nonspecific & less picky • Can eliminate a variety of infected/cancerous cells by detecting general abnormalities such as the lack of 'self' cell-surface proteins (MHC) • Not phagocyte - kill directly by contact, inducing apoptosis • Secrete potent chemicals that enhance inflammatory response Inflammation - Tissue Response to Injury • Triggered when tissues are injured • Beneficial effects o Prevents spread of damaging agents o Disposes cell debris & pathogens o Alerts adaptive immune system o Sets stage for repair Inflammatory Chemical Release • Begins with flood of inflammatory chemicals released into extracellular fluid • Released by injured/stressed tissue & immune cells • Can also be formed proteins circulating in the blood (Ex. Mast cells release histamine) • Macrophages have membrane receptors allowing them to recognize invaders • These surface membrane receptors (TLRs) trigger immune responses • Once activated, a TLR triggers release of cytokines • Other inflammatory chemicals include kinins, prostaglandins & complement • All dilate local arterioles & make local capillaries leakier & attract WBCs to injured area Vasodilation & Increased Vascular Permeability • Redness & heat due to hyperemia (congestion with blood) occurs with dilation • Inflammatory chemicals also increase permeability of local capillaries • Exudate - fluid with clotting factors &Ab+ - seeps from blood --> tissues, causing edema, which presses on nerve endings (pain) • Surge of protein rich fluids into tissue sweets foreign material into lymphatic vessels for processing in lymph nodes • Also delivers important proteins (complement & clotting factors) to interstitial fluid • Clotting factors form a clot that acts as a scaffold for permanent repair & it isolates the injured area and prevents bacteria/harmful agents from spreading Phagocyte Mobilization • After inflammation, phagocytes flood damaged areas (neutrophils then macrophages) • If pathogens provoked the inflammation, complement is activated & elements of adaptive immunity also arrive at the injured site o Leukocytosis - leukocytosis induced factors are released by injured cells, neutrophils enter from red bone marrow. (Increase in WBCs) o Margination - inflamed endothelial cells sprout CAMs that signal "this is the place" so when neutrophils encounter CAMs, they steop & attach to it o Diapedesis - continued chemical signalling prompts neutrophils to flatten & squeeze between endothelial cells of capillary walls o Chemotaxis - WBCs migrate up gradient of chemotactine agents to the site of injury (positive) & within the hour, much foreign material at the site is devoured • After a while, monocytes arrive & become macrophages with large lysosomes, they replace neutrophils on the battle field Antimicrobial Proteins • Enhance innate defenses of attacking MO directly/hindering their ability to reproduce Interferons • Interferons help protect cells that haven't yet been infected • IFNs diffuse to nearby cells, which they stimulate to synthesize proteins that 'interfere' with viral replication in still-healthy cells by blocking protein synthesis & degrading viral RNA • Because IFN isn't virus-specific, IFNs produced against a particular virus protect against other viruses too • Family of immune modulating proteins produced by a variety of cells o Alpha & beta - antiviral effect ^ o Gamma - secreted by lymphocytes & has widespread immune mobilizing effects, such as activating macrophages Complement • Group of~20 plasma proteins that normally circulate in the blood inactively • C1-C9, factors B, D & P Fever • Abnormally high body temp - systemic response Adaptive Defenses • Body's built in specific defense system that eliminates almost any pathogen • Amplifies inflammatory response & is responsible for most complement activation • Unlike innate system, it must 'meet' or be primed by an intial exposure to a specific foreign substance (antigen) -- then it can protect the body o Specific - recognizes & targets particular pathogens/foreign substances o Systemic - immunity not restricted to initial infection site o Has memory - recognizes & mounts even stronger attacks on previously encountered pathogens • Humoral immunity (Ab+ mediated) - provided byAb present in the body's fluids • When lymphocytes defend the body, the immunity is cell-mediated immunity o Has cellular targets o Lymphocytes act against such targets either directly or indirectly Antigens • Substances that mobilize adaptive defenses & provoke immune response • Most are large & complex molecules CompleteAntigens & Haptens • Complete antigens have o Immunogenicity - ability to stimulate specific lymphocytes to proliferate o Reactivity - ability to react with the activated lymphocytes &Ab+ released by immunogenic reactions • Proteins are the strongest antigens • Small molecules are not immunogenic, but if they link up with the body's own proteins, the adaptive immune system may recognize the combination as foreign and mount an attack that is harmful rather than protective • The small molecule is an incomplete antigen Antigenic Determinants • Only certain parts of the antigen (antigenic determinants) are immunogenic • FreeAb/lymphocyte receptors bind to theseADs • Different lymphocytes 'recognize' differentADs, so a single antigen may mobilize several lymphocyte populations & stimulate formation of many kinds of antibodies • Large proteins have hundreds of chemically different antigenic determinants, which accounts for their high immunogenicity & reactivity Self-Antigens: MHC Proteins • Self-antigens aren't foreign or antigenic to you, but are antigen to other people • Among the cell surface proteins that identify a cell as 'self' is a group of glycoproteins called MHC proteins • Genes of MHC code for these proteins • Each MHC protein has deep groove that holds a peptide (self-antigen or a foreign antigen) • T-lymphocytes can only bind antigens that are presented on MHC proteins Cells of theAdaptive Immune System:An Overview • B lymphocytes - humoral immunity • T lymphocytes - non-Ab+ producing lymphocytes that constitute the cellular arm of adaptive immunity • APCs don't respond to specific antigens as lymphocytes do. Play essential auxiliary roles Lymphocytes Lymphocyte Development, Maturation & Activation • Originate in red bone marrow from hematopoietic stem cells • Educated: o Immunocompetence - must be able to recognize its one specific antigen by binding to it. When B/T cells become immunocompetent, they display a unique type of receptor on their surface which enables the lymphocyte to recognize & bind a specific antigen. They are committed to react to one distinctAD. Receptors on B cells are membrane-bound antibodies. o Self-Tolerance - Unresponsive to self-antigens • Primary lymphoid organs (thymus & bone marrow) • T cell education consists of positive & negative selection • Seeding secondary lymphoid organs & circulation • Antigen encounter & activation • Proliferation& Differentiation Generation of Antigen Receptor Diversity in Lymphocytes • Our genes, not antigens we encounter, determine which specific foreign substances our immune system will be able to recognize & resist • Antigen simply determines which existing T or B cells will proliferate & mount attack • Our lymphocytes make up to a billion types of antigen receptors -- specified by genes • Somatic recombination Antigen-Presenting Cells (APCs) • Engulf antigens & then present fragments of them on their own surfaces where T cells can recognize them • T cells can only be activated by antigens presented to them on MHC proteins byAPCs • Major types are dendritic cells, macrophages & B lymphocytes Dendr
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