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• Chapter 43 ~ The Body’s Defenses
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T CELLS.htm
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Overview• Three cooperative lines of defense• Defense against pathogens from food, air, water as
well as cancerous cells• Nonspecific: (innate)
– First Line: external– Second Line: internal
• Inflammation signals its action has been activated
• Specific: Third Line (acquired)– Immune System– Simultaneous with Second Line of Defense
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Lines of Defense
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I NONSPECIFIC DEFENSES
• .
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First Line of defense• External
– Prevents entry of microbes
• Skin– Physical barrier
• Mucous membranes-trap; ciliated epithelial cells sweep out mucus and trapped particulate – Trachea
• Secretions: Chemical defenses:• Oil and sweat glands create a low pH (skin 3-5)• Normal flora help maintain this low pH• Saliva, tears, mucous secretions contain antimicrobial proteins–
for example lysozymes• Stomach pH—exception is Hepatitis A virus
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Second Line of Defense
• First line broken….
• 1.Phagocytic white blood cells (leukocytes)
• 2.Antimicrobial proteins
• 3. Natural Killer Cells
• 4. The Inflammatory response
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1. Types of Phagocytic White Blood Cells• Neutrophils 60-70% WBCs;Enter infected cellsAttracted by chemicals released by infected cell engulf and destroy microbes inside infected tissue. Short life span—few days• Monocytes 5% WBCs Develop into macrophages Large; Long lived, use pseudopodia Digest microbeSome migrate; some strategically fixed—such as spleen,
lymph nodes and tissue
• Eosinophils 1.5% WBCs; destroy large parasitic invaders (parasitic
worms)Position themselves against invader-discharge enzymes
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• Natural killer (NK) cells• Don’t attack microbe directly• destroy virus-infected body cells & abnormal cells• Not phagocytes• Attack-cause cell lysis
• 2. Antimicrobial Proteins• 1. Complement Proteins—lysis results
• 2. Interferons-• Produced by virus-infected cells• Inhibit viral replication and activate natural killer cells• secreted by virus infected cells—limit cell-to-cell infection• Reproduced by recombinant DNA—being tested for treatment of
viral infections and cancer
Other Nonspecific Defenses
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The Inflammatory Response
• Occurs upon damage to tissue– Physical injury– Microorganism entry
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3.The Inflammatory Response (localized)• Tissue injury; release of chemical signals~ • most
common is histamine (basophils & mast cells): • Causing Vasodilation and increased permeability; • Prostaglandins released from WBC and damaged tissues
– This increases blood flow to injury
– Enhances delivery of clotting elements &more phagocyte( cells release chemokines attracts) :
• The Vasodilation and increased flow of blood causes characteristic reddening.
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4- Phagocytosis of pathogens~neutrophils arrive first, followed by macrophagesMacrophages destroy as well as clean up (pus) •
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Systemic Responses to more severe infection
Meningitis, appendicitisFever & Pyrogens: leukocyte-released molecules (pyrogens) increase body
temperature—sets body’s thermostat at higher temp.
High Temp: inhibits microbe growth; facilitate phagocytosis; speed up tissue repair
Septic ShockOverwhelming systemic responseHigh fever & low blood pressure Most common cause of death in U.S. non-coronary critical care
units
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II SPECIFIC IMMUNITY
• .
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Specific Immunity—Acquired Immunity
• Lymphocytes provide specific defense (special kinds of leukocytes)– B cells and T cells
• The Innate and acquired defenses interact---Helper T cells coordinate.
• Antigen: a foreign molecule that elicits a response by lymphocytes (virus, bacteria, fungus, protozoa, parasitic worms); usually a protein.
• Antibodies: circulating antigen-binding immunoglobulin, produced by B cells
• Antigen receptors: plasma membrane receptors on B and T cells
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• Ended here Friday
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APC- Antigen Presenting Cells
• Macrophages and B-Cells
• Display internalized antigens to Th cells.
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• Lymphocyctes• Develop from Pluripotent stem
cellsin bone marrow or liver of fetus.• Display specificity for a particular epitope (binding site) on an
antigen.• Recognize self from non-self cells
• 2 main types:– 1. B Cells – 2. T Cells (thymus)
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• B-Cells
--mature in bone marrow– Secrete antibodies (immunoglobulins)
– Recognize intact antigens (on whole microbes found while patrolling body fluids—blood/lymph)
– Humoral Response
– Also have membrane antibodies on surface
– APC-present antigens to Th, then they are activated and proliferate
– -----------------------------------------------
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T-Cells• mature in thymus• don’t secrete antibodies• 2 types
• cytoxic (killer) -T Cells– Function in Cell-Mediated Immunity– Infected cells, cancerous, foreign cells– Receptors for Class I MHC– CD8 protein enhances binding to Th cell for activation.
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Helper T-Cells
• Usually needed to activate B Cells & their proliferation– T-Dependent antigens
Have receptors for class II MHC proteins
CD4 protein enhances Th cell binding to B-cell in the humoral response.
Function in both types of immune responses:
1. Humoral (free invaders in body fluids)
2. Cell-Mediated (infected, defective, foreign cell)
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MHC• Major histocompatability complex
– Glycoproteins embedded in plasma membranes.– “self-markers”; Most polymorphic genes known
– 2 main classes:• Class I MHC: located on all nucleated cells
• Class II MHC: specialized cells: macrophages & B cells.• Function in antigen presentation-bind to antigen &
facilitate antigen binding to a T cell.
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Clonal selection- page 905Antigens interact with specific lymphocytes, inducing
immune responses and immunological memory
• Clonal selection: antigen-driven cloning of lymphocytes
• Antigen binds to receptor• “Selected” cell proliferates.• 2 “clones” of cells are produced.• 1.Effector cells: short-lived cells
that combat the antigen.• 2. Memory cells: long-lived cells
that bear receptors for the antigen.
• “Each antigen, by binding to specific receptors, selectively activates a tiny fraction of cells from the body’s diverse pool of lymphocytes; this relatively small number of selected cells gives rise to clones of thousands of cells, all specific for and dedicated to eliminating the antigen.”
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Induction of Immune Responses• Primary immune response: lymphocyte proliferation and differentiation the
1st time the body is exposed to an antigen.takes 10-17 days for max response.
During this time, selected B- cells generate antibody producing effector cells (clonal selection) called Plasma cells:
And Selected T-cells will produce effector T cells (no antibodies)• Secondary immune response: immune response if the individual is exposed
to the same antigen at some later time~ Immunological memory• Faster, more intense, longer than Primary
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2 Types of immune responses• Humoral immunity• B cell activation• Production of antibodies• Microbes circulating in blood
and lymph (body fluids)• Defend against free bacteria,
toxins, and viruses in body fluids.
• Cell-mediated immunity• Tc cell activation• Binds to and/or lyses cells• Defend against cells infected
with bacteria, viruses, fungi, protozoa, and parasites; nonself cells, cancer.
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Helper T cells—bring on the calvary• Function in both humoral (antibody production) & cell-mediated immunity• Activated by antigen presenting cells (APCs) bearing the class MHCII molecule• CD4 (Th surface protein), enhances activation, as does
Interlukin 1 (IL-1) .• Once activated, it proliferates, clone forms, Interlukin II (IL-2)further stimulates and helps
activate B-cells and Tc• Cytokines secreted (stimulate other lymphocytes): a) interleukin-2 (IL-2):
activates B cells and cytotoxic T cells b) interleukin-1 (IL-1): activates helper T cell to produce IL-2
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Cell-mediated Immunity:cytotoxic T cells• Destroy cells infected by intracellular pathogens and cancer cells• Infected cell displays antigen (pieces of pathogen) on its….• Class I MHC molecules • Activity enhanced by CD8 surface protein present on most cytotoxic T cells (similar to CD4 and class II MHC)• TC cell releases perforin, a protein that forms pores in the target cell membrane; cell lysis and pathogen
exposure to circulating antibodies
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Antibody Structure & Function• Globular serum proteins
• Epitope: region on antigen surface recognized by antibodies
• 2 heavy chains and 2 light chains joined by disulfide bridges
• 2 Antigen-binding sites (variable region)
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5 classes of Immunoglobins• IgM: 1st to circulate; First to respond to
infection. indicates current infection; too large to cross placenta
• IgG: most abundant; crosses walls of blood vessels and placenta; protects against bacteria, viruses, & toxins; activates complement
• IgA: produced by cells in mucous membranes; prevent attachment of viruses/bacteria to epithelial surfaces; also found in saliva, tears, and perspiration
• IgD: do not activate complement and cannot cross placenta; found on surfaces of B cells; probably help differentiation of B cells into plasma and memory cells
• IgE: very large; small quantity; releases histamines-allergic reaction
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Abnormal immune function• Allergies (anaphylactic shock): hypersensitive responses to environmental antigens
(allergens); causes dilation and blood vessel permeability (antihistamines); epinephrine
• Autoimmune disease: multiple sclerosis, lupus, rheumatoid arthritis, insulin-dependent diabetes mellitus
• Immunodeficiency disease: SCIDS (bubble-boy); A.I.D.S.
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Antibody-mediated Antigen Disposal• Neutralization (opsonization): antibody binds to and blocks antigen activity• Agglutination: antigen (and microbe) clumping• Precipitation: cross-linking of soluble antigens (proteins)• Complement fixation: activation of 20 serum proteins, through
cascading action, lyse viruses and pathogenic cells.– MAC attack
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Immunity in Health & Disease• Active: naturally acquired : conferred
immunity by recovering from disease
• Active: artificially acquired: immunization and vaccination;
produces a primary response & memory
• Passive immunity: transfer of immunity (antibodies) from one individual to another.
• Short term—weeks to months
natural: mother to fetus via breast milk
artificial: rabies antibodies
• ABO blood groups (antigen presence)
• Rh factor (blood cell antigen); Rh- mother vs. an Rh+ fetus (inherited from father). IgG
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