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Chapter 22 Notes Cont'd

by: Gail Chernomorets

Chapter 22 Notes Cont'd BIOL 224

Gail Chernomorets

GPA 3.2

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Notes from 10/11 & 10/13 Includes the Table and Figures from the book listed in the powerpoint
Human Anatomy and Physiology II
Sean Neiswenter
Class Notes
Anatomy & Physiology II
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This 16 page Class Notes was uploaded by Gail Chernomorets on Friday October 14, 2016. The Class Notes belongs to BIOL 224 at University of Nevada - Las Vegas taught by Sean Neiswenter in Fall 2016. Since its upload, it has received 15 views. For similar materials see Human Anatomy and Physiology II in Biology at University of Nevada - Las Vegas.


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Date Created: 10/14/16
Notes from 10/11 & 10/13 22 Cont’d T cells (cont’d)  Approximately 80% of circulating lymphocytes  Memory T cells - long term effect - vaccines come into play  B cells - make up 10-15% of circulating lymphocytes B cells  Make up 10-15% of circulating lymphocytes  Plasma cells - when stimulated, B cells can differentiate into plasma cells, which produce and secrete antibodies - activated form produce and secrete antibodies NK cells (Natural killer)  NK cells make up the remaining 5-10% of circulating lymphocytes  Similar to cytotoxic T cells - actively attacking cells, don’t target specific antigens, anything that is recognized as foreign - grouped with innate community (destroy anything foreign) Life Span and Circulation of Lymphocytes  Tissues maintain different T cell and B cell population - blood cell that spends time in other tissues  All types of lymphocytes move throughout the body - throughout tissues is where it is found - use blood/lymph for transport  most time not spent in blood, just use it - T cells  30 min in blood  6 hours in spleen  20 hours in lymph node  80% survive 4 years, some last 20+ - heavily based in lymph system Lymphopoiesis  Lymphocyte production  Location of maturation - red bone marrow - thymus - lymphoid tissues  Lymphoid stem cells - from hemocytoblasts  One type stays in red bone marrow - mature in - divides to produce NK cells and immature B cells - need exposure to hormones  B cell maturation requires - contact with stromal cells and exposure to hormones  Other type of stem cell matures in thymus - thymic hormones regulate further cell divisions - produce various T cells  RBC  thymus: immature still  Process matures it Lymphoid Tissues  Tissues dominated by lymphocytes  Lymphoid nodule - lymphocytes packed in areolar tissue - no capsule, clumped distribution  Found in - opening to the outside world - respiratory, digestive, urinary, reproductive systems - lymph nodes and spleen  ~ 1 mm across, indistinct boundary  Germinal center - dense dividing lymphocytes Mucosa-associated lymphatic tissue (MALT)  Lymphoid tissues that protect the epithelia - digestive, respiratory, urinary, reproductive systems  Also known as Peyer’s patches, appendix, and tonsils Tonsils  Large lymphoid nodules in the walls of the pharynx (throat) - important for immune system identification - most people have 2 palatine tonsils, one pharyngeal tonsil, and 2 lingual tonsils Lymphoid organs  surrounded by a fibrous connective tissue capsule  lymph nodes  thymus  spleen Lymph nodes  Has its own blood supply  First response to infection  Have lymphatic, drain areas; large lymphatic when all branches join node is the middle of the junction  Dense connective tissue capsule surrounds each node  Trabeculae are bundles of collagen fibers extending from the capsule into the interior of the lymph node - split up interior space of lymph nodes  Slows flow down through tissue  The hilum is a shallow indentation where blood vessels and nerves reach the lymph node - where enter to the organ  Afferent lymphatics - carry lymph from peripheral tissues to the lymph node - enter the lymph node opposite the hilum  Efferent lymphatics - carry lymph to venous circulation and leave the lymph node at the hilum ** Does not bring O o2 gases to lymph nodes  Multiple afferent lymphatics and push out of large vessel Lymph flow and lymph node functions  Full of macrophages, dendritic cells, B cells, and T cells  Lymph nodes act as filters - 99% of the antigens and debris removed - almost everything in tissue is screened and sorted and identified  Lymph nodes provide an early warning - problems detected before they affect vital organs The Thymus  Located in the mediastinum and atrophies after puberty - may contribute to diminishing effectiveness of immune system in elderly individuals  Divided into two lymphatic lobes (right and left) that are further divided into smaller lobules  Each lobule consists of an outer cortex and a central medulla  Relative size at age 2, actual size at puberty  T cells in the cortex are actively dividing - mature toward medulla - exit via medullary blood vessels  The thymus produces a group of hormones: thymosins - regulate T cell development Spleen  Redundant/reserve organ  Doesn’t do any job specific to only this organ Functions of the Spleen 1. Removal of abnormal blood cells by phagocytosis (done by liver) 2. Storage of iron recycled from red blood cells (done by liver) 3. Initiation of immune responses by B cells and T cells (done by other lymphoid tissues and organs) 4. Good source of blood (collection) holds to side - can push 300 mL back into circulation Spleen anatomy  The spleen is in contact with the diaphragm, the stomach, and the left kidney Histology of the Spleen  Surrounded by a fibrous capsule  Red pulp contains many red blood cells as well as macrophages  White pulp resembles lymphoid nodules - phagocytes  The spleen is very fragile  trauma to the left abdomen can rupture the capsule  Spleenectomy  removal of the spleen The Lymphatic System and body defenses Two categories of defenses 1. Innate (nonspecific) defenses  natural killer cells  always work the same way against any type of invading agent  just block things or make it an unfavorable environment 2. Adaptive (specific) defenses  protect against specific pathogens and mount response accordingly  depend on activities of specific lymphocytes  specific resistance (immunity) develops after exposure to environmental hazards - T cells and B cells Innate (nonspecific) defenses  Innate defenses are present at birth  Prevent the approach, deny the entry, or limit the spread of microorganisms and other hazards 1. Physical barriers ex. skin 2. Phagocytes ex. cell eating 3. Immunological surveillance ex. NK cells 4. Interferons ex. antiviral protein 5. Complement – collection of proteins, when activated come together and punch holes in a cell and allows liquid to enter and ultimately explode the cell 6. Inflammatory response 7. Fever Physical barriers  lined with epithelial tissues  Skin – layers of keratinocytes - hair, sweat, and antimicrobial secretions - within barrier can add additional structures  Epithelial layers of internal passageways - mucus membranes - line outside and inside  digestive, respiratory, urinary, reproductive tracts - mucus protects and moves materials – inside  digestive and respiratory tracts (acidic)  slows down or stops materials –innate defense that can add specific defenses to - enzymes, antibodies (not distinct), and pH – outside Phagocytes  Remove cellular debris and engulf microbes 1. Microphages – little eaters  Include neutrophils and eosinophils  Leave bloodstream and enter tissues to fight infections - other WBCs - first thing: increase BP - short lived 2. Macrophages – big eaters  Larger and usually monocytes  Fix (maintain resident population in organs) or mobile (actively move around organs)  Function: engulf pathogens/materials - Degrade in lysosome  Release toxic chemicals to destroy pathogens  Show immune system what foreign agents are in the body Movement and phagocytosis  All macrophages - move through capillary walls (emigration) – leaving of an area - movement based on chemical concentration (chemotaxis)  positive toward higher concentration - must attach to the target using membrane receptors (adhesion)  initiates phagocytosis Immunological surveillance  Is carried out by natural killer (NK) cells - nonspecific, don’t differentiate between types of invaders  Activated NK cells 1. Identify and attach to abnormal cell (nonselective)  Secrete things to destroy  Attack bacteria, cancer cells and virus infected cells 2. Golgi apparatus in NK cell forms perforin vesicles  Between body cells or foreign cells 3. Vesicles release proteins called perforins (exocytosis)  Causes lysis  Secrete proteins and attack itself when you have “sick” cells ex. cancer cells ** doesn’t work on all cancers ex. AIDS 4. Perforins lyse abnormal plasma membranes  Needs to maintain protein composition in its system - end result: cell death Process (simplified) 1. Recognition and adhesion 2. Realignment and Golgi apparatus 3. Secretion of perforin 4. Lysis of abnormal cell Interferons  Protein messengers – paracrine signaling and beyond  Interferons released by virus – infected cell, lymphocytes, and macrophages  Interferon release triggers antiviral proteins - synthesized in healthy cells - interfere with viral replication  doesn’t work on all viruses - sends signal to surrounding cells and warns that it is infected  Virus – DNA/RNA in protein package and inject into the host  Clinically used as a way to combat hepatic C by reducing viral replication Complement System  In plasma  11 complement © proteins  “Complement” antibody action - antibodies mark a bacterial cell - complement forms pores in cell – lysis - enhanced phagocytosis - histamine release  Term comes from complementing antibodies (originally) Inflammation  Aka inflammatory response  Caused by damaged cells that release signaling molecules  Inflammation – localized tissue response to injury that produces swelling (extra hydrostatic pressure which causes more filtration), redness, heat, and pain - Increases blood flow to area, reduced resistance  Effects - slows spread of pathogens - mobilization of local and systemic defenses  bring in nutrients - facilitation of repairs (regeneration)  Decrease blood flow to surrounding area The Response to Injury  Mast cells - release histamine, heparin and others - mechanical or chemical stress  Histamine - increases capillary permeability and blood flow  Increased blood flow - to and from site - increases the temperature  Clotting factors and complement proteins enter the area - clotting isolates area  plug hole, stop leak - complement attracts phagocytes  Neutrophils – first responders  Macrophages after – clean up crew  Cytokines from phagocytes - stimulate fibroblasts – forms scar tissue - repair area  Over time – fibrinolysis and regeneration Fever  Innate defense  Body temperature is maintained above 37 degrees Celsius (99 F)  Pyrogens are proteins that increase the set point for body temperature  Fever can be beneficial - some bacteria and viruses are inhibited by high temperature - 1 degree Celsius increase in body temperature = 10% increase in metabolic rate  tissue defenses function more rapidly Adaptive (Specific) Defenses  Born with the ability to develop it  Respond to individual threats and are either cell-mediated or antibody-mediated  Blocks almost everything from getting through  Can identify a single pathogen  Coordinated action of T cells and B cells  Cell-mediated immunity - occurs as T cells defend against abnormal cells and pathogens inside cells - actively target other cells  Antibody-mediated immunity - occurs as B cells defend against pathogens in body fluids - know what antigen and create antibody toward it Forms of Immunity Adaptive Immunity (acquired immunity)  Active Immunity - develops in response to antigen exposure 1. Naturally acquired active immunity  Develops after exposure to antigens in environment  Typical immune response  Acquired from natural infection  Refers to whatever target is if you’re developing an immune response to antigens 2. Artificially induced active immunity  Develops after administration of an antigen to prevent disease  Acquired from exposure purposely  Example: vaccine  “human induced”  Passive Immunity - produced by transfer of antibodies from another source 1. Naturally acquired passive immunity  Conferred by transfer of maternal antibodies across placenta or in breast milk  Example: hemolytic disease of newborn - mother Rh+ blood exposure - antibodies that cross placenta are passively acquired  something/one else is creating immunity and passes it to you 2. Artificially induced passive immunity  Conferred by administration of antibodies to combat infection  Tough  Example: anti-venom  artificially  inject a goat/rabbit with venom and they develop the antibodies - then gets injected into human with the already created antibodies Properties of Immunity 1. Specificity  Each T or B cell (millions of these) responds only to a specific antigen and ignores all others - Antigens are substances that stimulate the production of antibodies; toxins, bacteria, foreign cells  Anything that binds to or causes cells that have antibodies slighting different binding sites but all together - Only identifies one antigen (specific) - Specific target to antigen 2. Versatility  the body produces many types of lymphocytes  Each recognizes a different type of antigen  Active lymphocyte clones itself to fight specific antigen - days to weeks first response to antigen - whole army - some cells wont go on to become active cells; become memory 3. Memory  some previously activated lymphocytes (memory cells) stay in circulation  Provide faster, stronger, longer response if the same antigen is encountered again  Wait and search for familiar antigen  Hours to days for response 4. Tolerance  immune system ignores “normal” antigens (self)  Don’t destroy our own cells  Ways to remove cells that affect self antigens  protects against autoimmune diseases Review of Major Types of T cells 1. Cytotoxic T cells (T Cells) • Directly attack foreign antigens • Responsible for cell-mediated immunity • Toxic to other cells 2. Memory T cells • Clone more of themselves in response to “remembered” antigen • Larger and faster response • Actively go around and increase sensitivity when activated 3. Helper T cells (T Hells) • Stimulate function of T cells and B cells 4. Suppressor T cells (T cSlls) • Inhibit function of T cells and B cells • After response clears infection (week later) T Cells and Immunity  Before an immune response can begin, T cells must be activated by - Exposure to an appropriate antigen which involves  Antigen presentation  Antigen recognition - first signal - cell finds what it recognizes - antigen and recognize – binds to antigen - Costimulation  Second signal  Confirms that it is an infection  If 2ndsignal is never received the cell will kill itself - only recognizes antigen - could think that it is binding to self antigen Antigen Presentation  T cells only recognize antigens that are bound to specific glycoproteins in plasma membranes  MHC proteins - bind to antigens - have similar to MHC to family members  Class I MHC proteins - are found in the membranes of all nucleated cells - all except RBCs – tell that they belong and should not be destroyed - actively creating and sticking to membrane  Class II MHC proteins - present in the membranes of antigen-presenting cells and lymphocytes only when the cell is processing antigens - handful of specific cells; mostly macrophages - cleans up and processes parts - any antigens will be taken and incorporated in MHC protein and presented to immune system - important in activating T cells  Major histocompatible complex - tissue compatibility - name from history of major transplant failure Class I MHC proteins  Picks up small peptides in the cell and carry them to the surface  T cells ignore normal peptides (tolerance)  Abnormal peptides or viral proteins activate T cells to destroy the infected cell  Mostly viruses and some bacteria  Transcription/Translation into protein and fold into EC, while doing it the proteins get folded into it and sticks to cell membrane  Normal cell – no problem  If the cell becomes infected, foreign antigens incorporated - signal with foreign antigen causes an identification then it comes and clears it up  The abnormal peptides are displayed on the plasma membrane - way cell notifies immune system something is infected ** Infection is inside the cell Class II MHC proteins  Holds antigenic fragments from antigenic processing of pathogens  Antigen-presenting cells (APCs) - macrophages and dendritic cells - Activate T cells with foreign cells and proteins  Difference from Class I - where the infection is - during processing and present to immune system ** Infection is outside the cell Antigen Recognition  Cluster of differentiation recognize MHC proteins  T cells have receptors called CD markers  Bind either Class I or Class II MHC  CD markers have specific antigen binding site - each is different recognition - recognize class I or II  Specificity - only T cells capable of binding a particular antigen will be activated in response to the presentation of that antigen - if doesn’t, then it moves on  Over 70 different types - CD8 and CD4 are important in T cells Two Important CD Markers 1. CD8 Markers  Found on cytotoxic T cells and suppressor T cells  Respond to antigens on Class I MHC proteins 2. CD4 Markers  Found on helper T cells  Antigen allows recognition  Respond to antigens on Class II MHC proteins  Respond to macrophages or other lymphatics  For T cell to be activated, it must be costimulated -additional signal necessary -can be protein binding between T cell and stimulating cell -can also be chemical signals -confirms the cell is infected or an active phagocyte Activation of CD8 T cells  Two types of CD8 T cells are activated by exposure to antigens on Class I MHC proteins  One type responds quickly: - metabolism jumps up and divides (makes clones) - Cytotoxic T cells seek out and immediately destroy target cells - Memory T cells remain inactive (differentiating) in circulation to facilitate faster response if the antigen is encountered again (memory) - Stay back and used for future use - In first infection they are inactive, then become active if infected again  The other responds slowly, producing suppressor T cells - Suppressor T cells inhibit T cells and B cells which limits the immune response to a single stimulus - Week later - Reduce activity of cytotoxic cells Process simplified: 1. Antigen recognition 2. Costimulation 3. Activation and cell division 4. Destruction of target cells  Perobin release - disrupt membrane  Cytokine release - program cell death  Lymphotoxin - toxic chemicals disrupt metabolism End Result: cell destroyed with infection Activation of CD4 T cells  T cell receptor/Class II MHC binding and costimulation activate CD4 T cells  Active cells divide to produce - Active helper T cells (TH)hat secrete cytokines  Large group od signaling molecules  Activate T cell and B cell molecules - Memory helper T cells that remain in reserve ** Active helper T cells secrete cytokines that stimulate both cell- mediated and antibody-mediated immunity Functions of Cytokines 1. Stimulate T cell divisions  Produce memory T celHs  Accelerate cytotoxic T cell maturation 2. Attract and stimulate macrophages  If infection – macrophages move towards 3. Attract and stimulate activity of cytotoxic T cells  Come in and destroy 4. Promote activation of B cells Summary of MHC proteins  Antigen bound to Class I MHC protein  indicates that the cell is infected or otherwise abnormal  CD8 T cells  Cytotoxic T cells, Memory T cells, Suppressor T cells c  Antigen bound to Class II MHC protein  indicated presence of pathogens, toxins, or foreign proteins  CD4 T cells  Helper T cells, Memory T ceHls B Cell Sensitization and Activation • Millions of B cell populations present - Versatility - That respond to some thing different (each) • Each B cell carries its unique antibody - Specificity • B cells must first be sensitized - Antigen binds to correct B cell antibodies - Antigen taken into B cell - Bound to class II MHC proteins - Antigen Presentation • Helper T cells (activated via antigen presentation) stimulates to secrete cytokines to costimulate the sensitized B cells (2 nd signal that B cells need) • Activated B cells divide and differentiate • Plasma cells - produce and secrete antibodies • Memory B cells - rema - is inactive Antibody Structures  Two parallel pairs of polypeptides - one pair of heavy chains - one pair of light chains - the 5 classes of antibodies have different heavy chains  Each chain contains constant segments and variable segments  “Y” shape is the most common shape  The constant segments is the same among all antibodies and is what allows us to recognize our own antibodies Antibody Structure  Variable segments of light and heavy chains determine specificity of the antibody  Free tips of the two variable segments form the antigen binding sites of antibody molecule  binds to specific locations on the antigen called antigenic determinant sites Classes and Actions of Antibodies  The five classes of antibodies are also called immunoglobulins (Igs) - IgG, IgD, IgE, IgM, IgA  Classes are determined by structure of the heavy-chain constant segment  Antibodies of different classes can have the same binding specificity (same antigen binding sites)  Within a single plasma cell the variable is the same and constant differs - can produce all 5 so same antigen binding site  Variable region is the same in B cells - ability to produce any of the 5 - over time: can produce all of them ** Do not need to know what each is used for ** Only need to focus on IgG and IgM - IgG is small enough to get through every tissue; most common - IgM is the first cell produced and secreted; easy to make Problem: large; cant go through bloodstream Elimination of Antigen  Many are innate defenses  Formation of antigen-antibody complexes eliminate the antigen by:  ** KNOW the 7 ways 1. Neutralization  Of antigen binding sites makes viruses/toxins incapable of entering cells  Active site of toxin is blocked so no longer toxic 2. Precipitation and agglutination  Leads to the formation of immune complexes targeted for degradation  Bind up with antibodies  Viruses just put a cover 3. Activation of complement leads to cell lysis  Discovered as antibody attachment  Binds enzyme to antibody and starts punching holes which leads to lysis 4. Attraction of phagocytes leads to degradation  Binded to constant region 5. An antibody coating (opsonization) increases phagocyte efficiency  Flagging cell for destruction 6. Stimulation of inflammation 7. Prevention of bacterial and wiral adhesion by antibodies dissolved in saliva, mucus, and perspiration  Sticks to viruses/bacteria  Block from entering Primary and Secondary Responses to Antigen Exposure  Occur in both cell-mediated and antibody-mediated immunity  First exposure to antigen produces the primary response  Next exposure triggers a secondary response - More extensive and prolonged  memory cells The Primary Response  Takes time to develop as antigens activate B cells and activated B cells divide and differentiate  Antibody titer (level) slowly rises and may take 2 weeks to reach peak levels  IgM, although less effective, is produced more rapidly than IgG The Secondary Response  Activates memory B cells - at lower antigen concentrations than original B cells - secrete antibodies in massive quantities much faster Summary of the Immune Response  Combined Responses to Bacterial Infection  Neutrophils and NK cells begin killing bacteria - first response  Cytokines (signaling molecule) draw phagocytes to area - Ex. macrophages  Antigen presentation activates helper T cells and cytotoxic T cells - those populations become active, takes several days (highly virulent)  B cells activate and differentiate  Plasma cells increase antibody levels Combined Responses to Viral Infection  Similar to bacterial infection  But cytotoxic T cells and NK cells are activated by contact with virus-infected cells  **Bacteria outside cell Table 22-2 Figure 22-26 Figure 22-27


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