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UMass Amherst MICROBIO 310 - Immune Mechanisms

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Microbio 310 1st Edition Lecture 26 Outline of Last Lecture I. 28.5 InflammationII. 28.6 Natural ImmunityIII. 28.7 Artificial Immunity and ImmunizationIV. 28.9 Allergy, Hypersensitivity, and AutoimmunityV. 28.10 Superantigens: Overactivation of T cellsOutline of Current Lecture I. 29.1 Innate Response Mechanisms II. 29.2 Adaptive Response Mechanisms III. 29.3 Immunogens and Antigens IV. 29.4 Antigen Presentation to T Cells V. 29.5 T-Cytotoxic Cells and Natural Killer Cells VI. 29.6 T-Helper Cells Current Lecture29.1 Innate Response Mechanisms• Innate immunity– Body’s built-in ability to recognize and destroy pathogens or their products • Innate immune response is the first line of defense : – Begins when phagocyte encounters a pathogen or pathogen product These notes represent a detailed interpretation of the professor’s lecture. GradeBuddy is best used as a supplement to your own notes, not as a substitute.: – Inflammation can result • Phagocytes engulf and destroy pathogens : – Include macrophages, monocytes, and neutrophils : – Move by amoeboid action and have lysosomes : – Trap and engulf pathogens on surfaces - Neutrophils are actively mobile granulocytes - Monocytes are precursors of macrophages – Large cells found in tissues such as lymph nodes and spleen- Dendritic cells function in phagocytosis and antigen presentation – When they ingest antigen they move to the lymph node to present antigen to T cells • Phagocytes recognize a pathogen using pattern recognition receptors (PRRs) – Membrane-bound phagocyte proteins that recognize pathogen-associated molecular patterns (PAMPs) • Toll-like receptors (TLRs) recognize PAMPs • The activation of certain genes in phagocytes enhances their phagocytic and pathogen-killing abilities – Phagocytic cells use toxic oxygen to kill ingested bacterial cells by oxidizing key cellular constituents – Occurs within the phagocytic cell, which is not damaged by the toxic oxygen products • Inflammation is a nonspecific reaction to noxious stimuli – Redness, swelling, pain, and heat localized at site of infection • Molecular mediators of inflammation are proteins called cytokines and chemokines – Effective inflammatory response isolates and limits tissue damage, destroying damaged cells and pathogens – Inflammation can result in considerable damage to healthy tissue • Some pathogens have developed mechanisms for neutralizing toxic phagocytic products– Staphylococcus aureus and Mycobacterium tuberculosis• Some intracellular pathogens produce leukocidins that kill the phagocyte– Streptococcus pyogenes and S. aureus• Some bacteria produce a capsule resistant to phagocytosis– Streptococcus pneumoniae29.2 Adaptive Response Mechanisms• T lymphocytes recognize the peptide antigens through cell surface T cell receptors (TCRs)• In cell-mediated immunity, pathogen-infected host cells are killed after they are recognized viapathogen antigens found on their surface• Antibody-mediated immunity is effective against extracellular pathogens such as bacteria and soluble pathogen products (involves B cells)• Specificity of antigen–antibody reaction is dependent on lymphocyte cell receptors interactingwith individual pathogen/antigen via direct molecular interactions• Memory: subsequent exposures to the same antigen result in rapid production of large quantities of antigen-reactive T cells or antibodies (faster and stronger immune response)• Tolerance: the acquired inability to make an adaptive immune response to one’s own antigens. Immune cells are not able to react with self-antigen. – Self-reactive cells are destroyed during development of the immune system – Discrimination between foreign and host antigens29.3 Immunogens and Antigens• Several extrinsic factors influence immunogenicity – Dose of immunogen– Route of administration– Foreign nature of the immunogen with respect to the host29.4 Antigen Presentation to T Cells• T cell receptor (TCR) is a membrane-spanning protein – Each T cell has thousands of copies of the same TCR on its surface– Functional TCR consists of two polypeptides (alpha and beta chains)• Major histocompatibility complex (MHC)– Initially identified as being responsible for immune-mediated organ transplant rejection– Function as antigen-presenting molecules• Class I MHC on surface of all nucleated cells (present on every cell)• Class II MHC on B lymphocytes, macrophages, and dendritic cells– Specific to cells doing antigen presentation• MHC proteins expressed on the cell surface reflect the composition of the proteins inside the cell• Cells that have ingested foreign proteins or pathogens and cells infected with virus produce peptides that interact with MHC proteins• TCRs of a given T cell bind only to MHC molecules having foreign antigens embedded in the MHC structure• T cells do not interact with a foreign antigen unless it is presented in the context of a MHC protein29.5 T-Cytotoxic Cells and Natural Killer Cells• T-cytotoxic cells (CTLs or TC) are T cells that directly kill cells that display surface foreign antigens– Contact between TC cells and target cell is required for cell death– On contact, granules in T cell migrate to contact site– Degranulation (contents of granules are released) occurs and causes pores (perforin) intarget cell membrane– Also contain granzymes that cause apoptosis (programmed cell death)– Cells lacking antigen are not killed• Natural killer cells (NK cells) are distinct from T cells and B cells– Destroy cancer cells and cells infected with intracellular pathogens; use granzymes andperforin– Kill in the absence of a specific protein• Lack of normal MHCs result in killing (cell death by apoptosis)– No prior exposure to foreign cells required– Not enhanced and do not exhibit memory with target cells– NK cells are much less prevalent than cytotoxic T-cells29.6 T-Helper Cells• TH1 subset activates macrophages– Secrete cytokines (including gamma interferon and others)– Activated macrophages kill intracellular bacteria (increased phagocytosis of all pathogens)– Also play a role in inflammation and transplanted organ rejection• TH2 subset plays a crucial role in B cell activation and antibody


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