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Biology 162 Animal Immune System Lecture

by: Jenn Guzman

Biology 162 Animal Immune System Lecture Biology 162

Jenn Guzman
Cal Poly
GPA 3.3

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About this Document

These notes cover the last week of lecture for Dr. Taylor's Biology 162 course! She discussed the animal immune system, its function, general structure, as well as the role of vaccines.
Intro to Organismal Form and Function
Dr. Taylor, Dr. Ritter
Class Notes
Biology, Bio162, immune, system, animal, Dr.Taylor, week, 10, Lecture Notes
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This 4 page Class Notes was uploaded by Jenn Guzman on Wednesday June 1, 2016. The Class Notes belongs to Biology 162 at California Polytechnic State University San Luis Obispo taught by Dr. Taylor, Dr. Ritter in Spring 2016. Since its upload, it has received 10 views. For similar materials see Intro to Organismal Form and Function in Biological Sciences at California Polytechnic State University San Luis Obispo.

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Date Created: 06/01/16
Wednesday, June 1, 2016 Animal Immune System Week 10 Lecture Notes I. Overview of the Immune System A. Innate Immunity: already present when one is born; do not need to be exposed to a foreign pathogen; components include barriers (i.e. skin), leukocytes (white blood cells), fever (to create unfavorable conditions for the pathogen), and inflammation B.Adaptive Immunity: specific cells within the body activated by specific pathogens 1.umoral Adaptive Immunity: anything that kills pathogens located in the blood stream, that has otherwise not infected cells and remains extracellular; includes B lymphocytes (produce antibodies) 2. Cell-Mediated Immunity: cells already infected with the pathogen are attacked by T lymphocytes (T cells) II. Inflammatory Response of the Innate Immunity A.Pathogens enter the wound B. Platelets initiate blood clotting. C.Injured tissues and macrophages release chemokine that help recruit other immune response cells. D.Mast cells are stimulated to release histamines that constrict the blood vessels leading away from the wound, while nearby vessels to the wound are dilated Blood flow to the wound is greater than the blood flow away from it, both used to attack the pathogen and prevent it from spreading throughout the body. E.Neutrophils arrive at the wound and begin phagocytizing pathogens. Monocytes arrive and mature into macrophages. F.Cytokines induce fever and attract more cytokines. 1 Wednesday, June 1, 2016 III. Bone Marrow: constantly making B/T Lymphocytes A. DNA responsible for coding the receptors of these lymphocytes cells is constantly undergoing genetic recombination; as a result, millions of random protein receptor types are made so each may potentially match a pathogen into the body; all are continuously waiting to be activated 1. Antigens : identification proteins on a cell/pathogen body (ON EVERYTHING) a) Autoimmune Disease: lymphocytes randomly synthesize antigens compatible with self-cells that fail to be “filtered out” by the thymus or other immune system organs; includes Type I diabetes, multiple sclerosis, etc. 2. Lymphocytes recognize antigens via “lock and key” mechanism : the antigen is the “key” that “unlocks” the receptor cell’s “key”, causing the immune cells to now become activated and replicated millions of times over to overwhelm the pathogen a) There are three main types of inactive T-lymphocytes: B cell, CD4+, CD8+ b) Activated Lymphocytes include plasma cells, helper T cells, and cytotoxic T cells (1)Lymphocyte activation involves a huge increase in the amount of rough endoplasmic reticulum , increasing the amount of protein synthesis to fight the pathogen in the production of antibodies B.T-Cell Activation 1. Dendritic cell recognizes/engulfs/breaks up a pathogen, and presents pieces of the pathogen on its MHC proteins. CD8+ T cell receptors bind to MHC class I antigens, should it be a perfect match as a result of the genetic recombination. CD4+ T cell binds to MHC class II antigen. For CD8+ cells, the activated T cells multiply and 2. differentiate, entering the blood stream as cytotoxic “killer” T cel. 3. For CD4+ cells, those that are activated form Helper T cells that produce cytokines. IV. Cell-Mediated Response A. Cytotoxic T cell recognizes and binds infected 2 Wednesday, June 1, 2016 cell. B. T cell secretes pore-forming proteins and other proteins that are transported into the infected cell. C. Infected cell breaks up into fragments. Phagocytic cells consume the fragments, highlighting how innate and adaptive immunity are complementary V. B Cell Activation A. B cell recognizes invader due to the involvement of MHC class II proteins. B. B ell then stimulates active T cell. Cytokines are released, and the B cell is now activated thanks to helper T cells. C. Activated B cell divides to produce plasma cells, which in turn produce antibodies. Antibodies are proteins of the same configuration as the antigens so that they may attack the pathogen) D. Antibodies then bind to the pathogen and destroy it in one of four ways, initiatinHumoral Responses . 1. Humoral Response is dependent upon the activation of the cells involved in the cell-mediated response . 3 Wednesday, June 1, 2016 VI. Memory and Response Mechanisms A. Memory B/T cells allow for the more intense recognition and fight against pathogens after the primary exposure to the pathogen itself. These cells consist of the secondary immune response. 1.Vaccines take advantage of immunological memory to protect against viruses by introducing a weakened version of the virus (i.e. small pox, polio, measles, mumps, etc.) 2.HIV infects and kills Helper T cells (CD4+), but in itself is not fatal. The progression of the infection eventually causes AIDS when left untreated, which is then fatal. Antibodies cannot be produced since chronic HIV infection have killed off enough of the CD4 cells. Antibodies cannot be produced since it affects the helper T cells. 4


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