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The Lymphatic System & Immunity
Chapter 17
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Immunity Innate Immunity- fast, non-specific and no memory
Barriers, pH extremes, Phagocytes & NK cells, fever, inflammation, complement, interferon Adaptive Immunity Slower, specific & has a memory Lymphocytes: T-cells & B-cells
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Lymphatic System Lymphatic tissue – Bone marrow
reticular connective tissue containing lymphocytes Bone marrow Lymph- interstitial fluid in lymphatic vessels Returns excess filtration from capillaries- to circulation Transport dietary lipids Maintenance & distribution- lymphoid organs Filter bacteria and help active defenses
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Figure 17.1
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Lymphatic Vessels Begin at lymphatic capillaries
Slightly larger than blood capillaries Overlapping cells like one-way valve Pressure will force fluid in Merge to form larger & larger vessels Thin walled and more valves than veins Periodically have lymph nodes Lymphocytes in capsuled structure thoracic duct L subclavian vein at junction with jugular R. lymphatic duct R. subclavian vein
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Figure 17.2a
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Figure 17.2b
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Lymphatic flow From tissue to veins
Pumped by muscle & respiratory pumps like venous return
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Figure 17.3
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Lymphatic Organs Primary lymphatic organs- stem cells divide & develop into mature B & T-cells Red bone marrow & thymus Secondary organs: immune responses occur Lymph nodes, spleen & lymphatic nodules
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Thymus Two lobed organ Posterior to sternum, medial to lungs & superior to heart T-cells divide & mature Self reactive cells are removed
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Lymph nodes Scattered throughout the body
Concentrated near mammary glands, axilla & groin Contain mature B-cells, T-cells dendritic cells and macrophages Filter lymph, trap foreign substances Macrophages & lymphocytes destroy most foreign substances
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Figure 17.4
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Spleen Between stomach & diaphragm
Contains blood filled venous sinuses and RBCs, macrophages, lymphocytes plasma cells & granular leukocytes destroys worn or defective blood cells & platelets Stores platelets attacks foreign substances in blood Fetal Hemopoiesis
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Innate Immunity- Barriers
Skin: Physical & chemical Epidermal structure & constant shedding Mucous membranes: Sticky mucus layer straps microbes, etc. and cilia move it out Fluids: tears, saliva, perspiration, nasal secretionss Dilute and antibacterial action Movement: flow of urine, defecation & vomiting
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Internal Defenses- Proteins
Interferons- interfere with viral reproduction in a cell Complement System Enhance other immune actions Break cell membranes Attract phagocytes Tag microbial cells for destruction Transferrins- bind iron & starve bacteria Antimicrobial peptides: lyse microbes
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Internal Defenses-Cells
Phagocytes specialized to ingest microbes and cellular debris Neutrophils Monocytes macrophages 5-10% of lymphocytes = Natural Killer (NK) Cells Destroy microbes & tumor cells Present in lymph nodes & red bone marrow
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Inflammation Response to tissue damage
Indicated by redness, pain, heat & swelling 1. damage mast cells, basophils & platelets release histamine increased permeability & vasodilation in blood vessels
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Inflammation (Cont.) 2. leakage of clotting proteins into tissue-
Isolate bacteria behind clot 3. phagocytes attracted to site Neutrophils & macrophages eat & die 4. pocket of dead cells = pus Moves to body surface or into cavity & is cleared
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Figure 17.5
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Fever Abnormally high body temperature
New set-point of thermoregulation system Normal temperature control action with new set point. Stimulated by many toxins or internal signals : interleukin-1
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Adaptive Immunity Specifically directed against a particular type of invader Involves cell or antibody directed against a particular antigen Antigen can be any substance: microbe, food, pollen, tissue Normally self–tolerant (does not attack normal body tissue)
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Maturation of T & B cells
From stem cells in red bone marrow B cells mature in bone marrow T cells migrate to thymus During maturation both make particular proteins in plasma membranes = antigen receptors
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Types of Responses Cell-mediated- T-cells attack directly
Killer T-cells Antibody-mediated- B cells become plasma cells produce specific antibodies Helper T cells aid both cell- and antibody-mediated responses
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Antigens & Antibodies Major Histocompatability Complex (MHC) = self antigens on cells surface Unique to each individual Allows T-cells to recognize foreign material Antigen triggers plasma cell to produce antibodies Y-shaped protein with variable antigen binding site on arms Other end triggers recognition by phagocyte
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Figure 17.6a
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Figure 17.6b
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Triggering Adaptive Response
requires recognizing the foreign antigen B-ceils can find it anywhere T-cells need presentation with MHC Antigen presenting cells (APC) do this APCs macrophages, dendritic cells & B cells In respiratory, GI, urinary, reproductive tracts & lymph nodes
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Processing & Presenting Antigens
APC’s ingest & digest into fragments in vesicles Synthesize MHC & pack in vesicles Two vesicles fuse antigen fragments bind to MHC Antigen-MHC complex inserted into plasma membrane Presented to T-cells until a receptor matches & binds
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Figure 17.7
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Cell Mediated Immunity
T-ceils also need costimulator Interleukin-2 (IL-2) Binding both response T-cell begins rapidly dividing Forms a clone of many recognizing cells Helper T cells- release IL2, attract phagocytes, stimulate macrophages & B cells Cytotoxic T cells – kill cells Work against tumor cells transplanted cells & infected cells Memory T cells- hang around for years, give rapid response
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Figure 17.8
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Figure 17.9
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B-cells and Antibody- Mediated Response
Hang out in lymph nodes Respond to antigen (faster if presented) With IL-2 enlarge, divide and become a clone of plasma cells Plasma cells produce & release antibodies that bind the antigen Some remain as Memory B Cells Ready to respond quickly if antigen met again
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Figure 17.11
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Antibody Class Actions
Neutralizing antigen- Binds & neutralizes toxins Immobilizing bacteria Agglutinating- Connect pathogens to one another easier phagocytosis Activating complement Enhancing phagocytosis Binding attracts phagocytes
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Immunological Memory Long lasting antibodies & lymphocytes
Many sensitive memory cells Much larger & quicker response next time = Secondary Response Primary response can be naturally acquired or artificially acquired by vaccination Killed cells, isolated antigens, parts of viruses
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Aging Thymus atrophies Fewer responsive T cells
Thus poorer B cell response Poorer response to new infection
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