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By : Pooja Patel & Sarah Gianopoulos. Innate immunity—nonspecific, used against many organisms:  First line of defense includes barriers, such as skin.

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Presentation on theme: "By : Pooja Patel & Sarah Gianopoulos. Innate immunity—nonspecific, used against many organisms:  First line of defense includes barriers, such as skin."— Presentation transcript:

1 By : Pooja Patel & Sarah Gianopoulos

2 Innate immunity—nonspecific, used against many organisms:  First line of defense includes barriers, such as skin and molecules toxic to invaders  Second line of defense includes phagocytic cells, which ingest foreign cells and particles  Most animals use innate immunity

3 Adaptive Immmunity—specific, used to distinguish between substances that were made by the organism or if they are foreign substances:  Uses antibody proteins to recognize, bind to, assist in destroying specific bacteria and viruses  Adaptive immunity is slow to develop and long lasting  Innate immunity is much quicker to develop (0- 96 hours)

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5  Phagocytes  Large cells that engulf pathogens and harmful substances  Lymphocytes  Include B and T cells  B Lymphocytes differentiate and form antibody producing cells and memory cells  T Lymphocytes kill the virus infected cells and regulate white blood cell activity

6  Cytokines bind to cell surface receptors and alter the behavior of their target cells  Some can activate or inactivate B and T cells and macrophages  Antibodies are proteins, produced by B cells that bind specifically to nonself substances  Acts as a flag to make it easier for the immune system cells to attack the invader  Destruction done by inactivating/destroying harmful pathogens, toxins and other microorganisms

7 Major histocompatibility complex (MHC) MHC proteins are important self- identifying labels that make sure the appropriate type of T cell binds during immune responses.  T cell receptors are integral membrane proteins on T cells, recognize and bind to nonself molecules

8  Skin  Rarely penetrated by bacteria  Skin’s saltiness is not an ideal environment for bacterial growth  Both harmless and helpful bacteria will have to compete for space and nutrients on the skin against pathogens and harmful substances

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10  Mucus  Traps microorganisms and pathogens and is carried away by cilia  Lysozome (enzyme)  Produced by mucus membranes and cleaves on the cell walls of the bacteria, thus making the harmful cell ‘lyse’  Use of internal substances

11  Defensins (peptides)  Made by mucus membranes  Hydrophobic and toxic to several other pathogens  Insert themselves into the plasma membrane to make the it permeable to water and solutes, thus killing the harmful substances

12  Phagocytes ingest the harmful substance and destroy it by 1 of 2 ways:  Hydrolysis within lysosomes  Defensins

13  Natural Killer Cells  Distinguishing between healthy and unhealthy cells ▪ Apoptosis for cancerous cells ▪ For other cells, Innate and Adaptive defenses combine by lysing antibody –labeled target cells

14  Complement Proteins  A system that activates several proteins in sequence in order to lyse the invaded cell ▪ One complement protein acts as a flag to the phagocytes as it binds to the invaded cells ▪ Next protein is activated to initiate the inflammation response and signals to the phagocytes to the infection site ▪ Then many other proteins now lyse the invaded cell

15  Interferons  Proteins that help increase resistance of neighboring cells to infection ▪ Bind to receptors on the plasma membranes of the uninfected cells to stimulate a pathway that inhibits viral reproduction the other cells become infected

16 Inflammation  Isolates the infected area to stop spreading the damage  Brings in cells and molecules to kill off any remaining pathogens and initiates the healing process  Mast cells are cells adhering to skin and organ linings; release chemical signals.  Tumor necrosis factor—cytokine that kills target cells and activates immune cells

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18  Adaptive Immunity is:  Specific  Diverse  Can distinguish between self and nonself substances ▪ Clonal deletion  Has immunological memory

19  Specificity:  T cell receptors and antibodies bind to specific nonself molecules (antigens).  Specific sites on the antigens are called antigenic determinants.  The host responds to an antigen’s presence with highly specific defenses using T cell receptors and antibodies.

20  Lymphocytes are usually activated by binding to antigens to induce production of clones of B Cells and T Cells-clonal selection.  To protect Self substances:  Clonal deletion—Any immature B and T cells that show the potential to mount an immune response to self antigens undergo apoptosis.

21  Primary Immune Response  Memory Cells  Secondary Immune Response  Produces a quicker and more powerful response

22 Recognition phase—the organism discriminates between self and nonself to detect a pathogen. Activation phase—the recognition event leads to a mobilization of cells and molecules to fight the invader. Effector phase—the mobilized cells and molecules destroy the invader.

23  Cytotoxic T (T C ) cells power the cellular immune response.  An antigen is inserted into the membrane of an antigen-presenting cell.  The antigen is recognized by a T-helper (T H ) cell, with a specific T cell receptor protein.  T H cell binding to the antigen-presenting cell causes cytokine release.  Cytokines stimulate T C cells to divide.

24  Humoral immune response involves B cells that make antibodies.  Antigen is recognized when the it binds to a B cell that has an antibody specific to that antigen.  Antigen binding readies a B cell for division.  The T H cell bound to the B cell secretes cytokines that stimulate the B cell to divide and form a clone.

25  The result of both types of immunities: A clone of B cells that can produce antibodies specific for the antigen A clone of T C cells that express a T cell receptor that can bind to any cell expressing the antigen on its surface  In the effector phase, B clone cells produce antibodies that bind to free antigen— results in inactivation and destruction of the antigen.  T C clone cells bind to cells bearing the antigen and destroy them.

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28  B cells give rise to clones of plasma and memory cells upon activation.  Plasma cells and B Cells secrete antibodies into the blood stream. Some bind to the antigen on surface of a pathogen. Some may use cross-linking function to form large complexes to be destroyed by phagocytes.

29  Antibodies all contain a tetramer of four polypeptides.  In each molecule are two light chains and two heavy chains, held together by disulfide bonds.  Each polypeptide chain has a constant region and a variable region.  The constant region determines the general structure and function of an immunoglobulin.  The variable region is different for each specific immunoglobulin—responsible for antibody specificity.

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32 IgG is secreted by B cells and constitutes about 80 percent of circulating antibodies. IgD is the cell surface receptor on a B cell. IgM is the initial surface and circulating antibody released by a B cell. IgA protects mucosa on epithelia exposed to the environment. IgE binds to mast cells and is involved with inflammation.

33  Each mature B cell can produce only one specific antibody with a specific amino acid sequence.  The B cell genome: Each gene encoding an antibody is a supergene assembled from many smaller genes.  During B cell development the genes are cut out and rearranged.  DNA is rearranged or mutated to create high diversity of antibodies.

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35  Cellular immune response involves: T-helper cells (T H ) Cytotoxic T cells (T C ) Histocompatibility proteins (MHC) proteins  T cells have specific membrane receptors— glycoproteins, with two polypeptide chains.  Each chain is encoded by a different gene  T cell receptors can bind a piece or fragment of an antigen, on the surface of an antigen- presenting cell.

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37  T C cells bind to cells carrying the antigen– MHC I protein complex.  When bound, the T C cells do two things to eliminate the antigen-carrying cell: They produce perforin, which lyses the bound target cell. They stimulate apoptosis in the target cell.

38  Regulatory T cells (Tregs) regulate the immune response.  Tregs recognize and mediate tolerance to self antigens — when activated they release the cytokine interleukin 10.  This blocks T cell activation and leads to apoptosis of T C and T H cells bound to the same antigen.

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40  Immune deficiency disorders can be inherited or acquired.  T or B cells may never form, or B cells lose their ability to give rise to plasma cells  Acquired immune deficiency syndrome (AIDS) results from infection by human immunodeficiency virus (HIV).

41  HIV initially infects T H cells, macrophages, and antigen-presenting dendritic cells.  Numbers of T H cells decline after infection.  HIV-infected cells activate the humoral immune system and symptoms abate.  During the dormant period, people with HIV feel fine.

42  Eventually more T H cells are destroyed and the person is susceptible to opportunistic infections: Pneumonia Lymphoma tumors Drug treatments for HIV are focused on inhibiting processes necessary for viral entry, assembly, and replication.

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