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BSC 216 Lymphatic and Immune System Part II

by: Vanessa Notetaker

BSC 216 Lymphatic and Immune System Part II BSC 216

Marketplace > University of Alabama - Tuscaloosa > Biology > BSC 216 > BSC 216 Lymphatic and Immune System Part II
Vanessa Notetaker
GPA 3.71

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Notes taken on September 22 (Thursday) The last six slides of this lecture were not covered in class so they will be included in the next upload with the Respiratory system. These notes include all...
Anatomy & Physiology II
Austin Hicks
Class Notes
Immunity, Anatomy & Physiology II, anatomy, Physiology
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This 8 page Class Notes was uploaded by Vanessa Notetaker on Monday September 26, 2016. The Class Notes belongs to BSC 216 at University of Alabama - Tuscaloosa taught by Austin Hicks in Fall 2016. Since its upload, it has received 18 views. For similar materials see Anatomy & Physiology II in Biology at University of Alabama - Tuscaloosa.


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Date Created: 09/26/16
BSC 216 Lymphatic & Immune System Part 2 Innate Defenses: The Complement System  Complement system o Group of about 30 proteins that work together to contribute to the nonspecific resistance and specific immunity o Synthesized mainly in the liver and circulate blood in the inactive form o Pathogen destruction is brought about through  Inflammation  Immune clearance  Phagocytosis  Cytolysis o Two routes of activation of the complement system  Classical pathway  Alternative pathway Classical Pathway  Requires antibody molecule to get started o Part of specific immunity  Antibody binds to antigen on surface of the pathogenic organism o Forms antigen-antibody complex  Changes the antibody shape at binding o Exposes pair of complement binding sites o Binding of first complement sets off a reaction cascade called the complement fixation o Antibody does not become active until C3 is cleaved into C3a and C3b Alternative Pathway  Nonspecific, part of innate immunity and does not require antibody  C3 breaks down in the blood to form C3a and C3b o C3 randomly breaks down without presence of cascade o C3b binds directly to targets such as human tumor cells, viruses, bacteria and yeasts o Also, triggers cascade reaction with autocatalytic effect where more C3 is formed but, this is after it is already initiated  Does not start in same way as classical pathway  Cascade reaction only occurs after C3 has been cleaved Mechanisms of Action of Complement Proteins  Inflammation o C3a stimulates mast cells and basophils to secrete histamine and other inflammatory chemicals  C3a binds to basophils and mast cells o Activates and attracts neutrophils and macrophages o Speeds pathogen destruction in inflammation  Immune clearance o C3b binds with antigen-antibody complexes to RBCs o RBCs with antigen-antibody complexes then circulate through the liver and spleen o Macrophages of those organs strip off and destroy the Ag-Ab complexes leaving RBCs unharmed o This is the primary means of clearing foreign antigens from the blood stream  Phagocytosis o Neutrophils and macrophages cannot phagocytize “naked” bacteria, viruses or other pathogens o C3b assists them by opsonization  Coats microbial cells and serves as binding cite for phagocytic cell attachment  Makes foreign cells more appetizing for phagocytic cells  Cytolysis o C3b splits other complement proteins o Bind to enemy cell o Attract more complement proteins so that membrane attack complex (MAC) form  Forms a hole in the target cell  Electrolytes leak out and water flows in rapidly, cell ruptures Innate Defenses: Inflammation  Inflammation-local defensive response to tissue injury of any kind, including trauma and infection o Suffix -itis denotes inflammation of specific organs  Purposes o Limit spread of pathogens and then destroys them o Removes debris from damaged tissue o Initiates tissue repair  Signs o Redness, swelling, heat and pain  Processes o Mobilization of Body defenses o Containment and destruction of pathogens  Containment gives leukocytes time to destruct the pathogens o Tissue clean up and repair Innate Defenses: Mobilization of Defenses  Most immediate requirement when injury occurs is to get the leukocytes to site ASAP o When the tissue is damaged some basophils and mast cells are already present and assist in leukocyte recruitment  Local hyperemia (increasing blood flow beyond normal rate) o Occurs via vasodilation via vasoactive chemicals  Histamine, leukotrienes and other cytokines  Histamines dilate postcapillary venules, increase vessel permeability and cause local edema (dilute harmful substances)  Cytokines promote inflammation and recruit WBCs  Secreted by basophils, mast cells, cells damaged by trauma, toxins, or other organisms triggering inflammation o Hyperemia also washes toxins and metabolic wastes from the site more rapidly  Cytokines are a class of chemicals that regulate inflammation and immunity o Secreted mainly by leukocytes o Alter the physiology or behavior of receiving cell o Act at short range, neighboring cells (paracrines) or same cell that secretes them (autocrines)  Vasoactive chemicals dilate local blood vessels o Endothelial cells separate, increasing capillary permeability o Fluid, leukocytes, and plasma proteins leave the bloodstream  Complement, antibodies and clotting proteins o Selectins: cell adhesion molecules made by the endothelial cells that aid in the recruitment of leukocytes  Make membranes sticky and snag leukocytes  Help leukocytes escape the blood by slowing them down  Neutrophil behavior o Margination  Selectins cause leukocytes to adhere to blood vessel walls o Diapedesis(emigration)  Leukocytes squeeze between endothelial cells into tissue space  Neutrophils are usually the first to respond Containment and Destruction of Pathogens  Priority of inflammation is to prevent the pathogens from spreading throughout the body o Fibrinogen that filters into tissue fluid clots  Forms a sticky mesh that walls off microbes  Plasma protein that ends as fibrin o Heparin prevents clotting at the site of injury  Pathogens are in a fluid pocket surrounded by clot so that ring of fibrin has fluid inside to kill the pathogen  Attacked by antibodies, phagocytes and other defenses  Neutrophils, the chief enemy of bacteria, accumulate at the injury site within an hour o After leaving the bloodstream they exhibit chemotaxis  Chemotaxis- attraction of chemicals such as bradykinin and leukotrienes that guide neutrophils to the injury site  Neutrophils are the quickest to respond and kill bacteria by o Phagocytosis o Respiratory burst o Secrete cytokines for recruitment of macrophages and additional neutrophils o Macrophages and T cells secrete colony stimulating factor to stimulate leukopoiesis  Neutrophils- 5000 cells/uL TO 25000 cells/uL in bacterial infection  Eosinophilla- elevated eosinophil count in allergy or parasitic infection Tissue Cleanup and Repair  Monocytes- the primary agents of tissue and cleanup repair  Arrive in 8-12 hours and become macrophages  Engulf and destroy bacteria, damaged host cells, and dead and dying neutrophils o There is much cellular debris to cleanup after injury  Edema contributes to tissue cleanup o Swelling compresses veins and reduces venous drainage o Forces open valves of lymphatic capillaries, promoting lymphatic drainage o Lymphatics collect and remove bacteria, dead cells, proteins and tissue debris better than blood capillaries  Pus is the accumulation of dead neutrophils, bacteria and cellular debris, and tissue fluid form a pool of yellowish fluid o Abscess: accumulation of pus in tissue cavity  Platelet derived growth factor- secretes by blood platelets and endothelial cells in injured area o Stimulates fibroblasts to multiply (mitosis) and synthesizes collagen  Hyperemia delivers oxygen, amino acids and other necessities for protein synthesis o Fuel for mitosis o Responsible for redness  Increased heat increases the metabolic rate, speeds mitosis, and tissue repair o Responsible for heat because of increased metabolism  Fibrin clot forms a scaffold for tissue reconstruction  Pain makes us limit the use of body part so it has a chance to rest and heal o Neurons terminating in the area of damage will be stimulated to limit movement Adaptive Immune System  Specific defense system (tailored, targeted attack)  Must come into contact with foreign substance (antigen) at least once prior to protecting body o Innate defenses can do serious damage to foreign substances on their first meeting  Two characteristics distinguish specific, adaptive immunity from nonspecific, innate resistance o Specificity: immunity directed against a particular pathogen o Memory: when re-exposed to the same pathogen, the body reacts so quickly that there is no noticeable illness  B and T cells remember previous attacks Two Major Branches of Adaptive Immune System  Cellular (cell mediated) immunity: T cells o Lymphocytes directly attack and destroy foreign cells or diseased host cells o Means of ridding the body of pathogens that reside inside human cells where they are inaccessible to antibodies o Kills cells that harb/or pathogens  Humoral (antibody mediated) immunity: B cells o Mediated by antibodies that do not directly destroy a pathogen o Antibodies mark infected cells for destruction- other immunity cells will then kill the cells “marked for death” o Can only work against the extracellular stage of infectious microorganisms  Difference between active and passive acquired immunity o Active immunity has to make antibodies according to introduced pathogen  Artificial is when a weakened antigen is introduced and body produces its own antibodies  Natural is acquired through exposure to infection o Passive immunity is the receiving of antibodies  Naturally acquired through breast milk of mother to child  Artificially acquired through injection of antibodies to toxins or venoms Antigens  Any “non-self” substance that can provoke an immune response  Epitope (antigenic determinant)- certain region of an antigen molecule that stimulates immune responses  Hapten- too small to provoke immune response o Once it combines with a host macromolecule and forms a complex it can become an antigen and provoke an immune response o Cosmetics, detergents, industrial chemicals, poison ivy and pet dander Cells of Adaptive Immunity 1. T lymphocytes are responsible for cell mediated immunity 2. B lymphocytes are responsible for humoral immunity 3. Antigen presenting cells (APC)  Immunocompetence- ability of a lymphocyte to recognize one specific antigen and bind to it  Self-tolerance- When lymphocytes learn about self-antigens and learn not to produce an immune response when exposed to them Educating the Lymphocytes  Before leaving the thymus lymphocytes need to be immunocompetent and have self-tolerance  They need to have self-recognition o If they produce a negative response (do not recognize self MHC) apoptosis occurs  MHC is a protein structure that is held out to immune cell to which binding can occur  Self- tolerance needs to be ensured o If T cell binds to MHC and reacts vigorously with self-antigen apoptosis is triggered  Only if the T cell recognizes the self-antigen and doesn’t attack is it allowed to leave the thymus and enter the bloodstream  B cells go through a similar exam in the bone marrow Antigen Presenting Cells  T cells cannot recognize their antigens on their own  Antigen Presenting Cells (APC) help the T cells recognize antigens o Dendritic cells, macrophages, reticular cells, and B cells function as APCs o APCs generally go through phagocytosis  Function of the APC depends on the type of major histocompatibility complex (MHC) proteins o MHCs act as identification tags that label every cell of body as belonging to that body o Structurally unique for each individual, except identical twins Self-Antigens  Major histocompatibility complex protein (MHC)- cell surface proteins that identify self  Class I MHC o Self-antigens o Found on all body cells o Can bind to pieces of material found within cells (protein breakdown) and “present” them at the cell surface  Class II MHC o Foreign antigens o Found only on cells that patrol the body and pick up antigenic material o Bind proteins that come from outside the cell and the patrolling cell presents the material at its cell surface The Action Antigen-Presenting Cells: Class I 1. The cell synthesizes a self-antigen 2. The antigen is broken down by enzymes in the cytosol 3. The antigen fragment is transported into the rough endoplasmic reticulum (RER) and is coupled with a class I MHC molecule in the RER membrane 4. The MHC antigen complex leaves the RER by a vesicle and is inserted into the cell’s plasma membrane The Action Antigen-Presenting Cells: Class II 1. The cell ingests a pathogen by phagocytosis 2. The phagocytic vesicle fuses with a lysosome: the pathogen is degraded and its antigens fragmented 3. The lysosome fuses with a vesicle from the RER that contains class II MHC molecules and an antigen fragment binds to the MHC molecule 4. The MHC antigen complex is inserted into the cell’s plasma membrane Cellular Immunity  Aka Cell Mediated Immunity  A form of specific defense in which the T lymphocytes directly attack and destroy diseased or foreign cells  The immune system remembers the antigens and prevents them from causing disease in the future  4 Classes of T cells Cellular Immunity: Four Types of T cells  Cytotoxic T (Tc) cells o Killer T cells o Effectors of cellular immunity that carry out the attack on enemy cells o Only T cells actually attacking  Helper T (TH) cells o Help promote T ccll and B cell action and nonspecific resistance3  Memory T (T )Mcells o Descend from cytotoxic T cells o Responsible for memory in cellular immunity o Can stay in the body for decades and are technically partially active cytotoxic T cells Cellular Immunity  Both cellular and humoral immunity occur in three stages o Recognition o Attack o Memory  Can be remembered as the three “Rs” of immunity o Recognize o React o Remember This chapter was not completed in lecture and the last six slides and notes will be included with Tuesday 9/27 notes on Respiratory System


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