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lec 3 blood and Immunity .doc

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Department
Physiology
Course Code
PSL201Y1
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Michelle French

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By: Farnaz Hosseini Blood and Immunity: Lecture 3 Innate Immunity (text book and lecture notes complied) (black-textbook and red- lecture notes added) Textbook chpt 23 page 668-675 Review from lecture 2: • Immunity refers to the immune system capacity to protect individual from disease by recognizing and eliminating pathogenic (disease generating) agents like bacteria, virus, parasites, and fungi • The immune system disposes unneeded components of the body like aging cells, debris, heals wounds, eliminates mutant cells that can become cancerous • It also has the ability to reject tissues and cells not identified to self (problem for organ transplantation) • These foreign substances induce the immune system to develop immune response- a complex series of physiological events accumulates in destroying them • Phagocytes- neutrophils, eosophils, monocytes, macrophages, dendritic cell are all in this category because they can engulf foreign substances removing them from the blood 1. Neutrophils are a lot in leukocytes fighting bacterial infections and elevation in neutrophils In blood is used to determine if the body has an infection. Neutrophils release cytokines creating inflammation 2. Eosiphils – these defend against parasite by releasing toxic molecules 3. Monocytes- these are phagocytes in blood but they differentiate into macrophages being 5-10x larger than monocytes and greater activity in tissue • Lymphocytes – they provide diversity, specificity, memory and ability to distinguish between self and non self • 3 major types: B cells (b lymphocytes), T cells and null cells (lack membrane components characteristic of B and T cells) • most null cells are large, granular, known as natural killer (NK) ] • when B cells contact foreign molecules known as antigen they then develop into molecules known as antigen where than they develop into plasma cells secreting antibodies called immunoglobulin • immunoglobulin- these are proteins in plasma and interstitial fluid targeting specific antigen for destruction • for example- B cell contacts bacteria aurous , develop into plasma cell secreting antibodies that only bind to aurous and mark them for destruction • T cells- these do direct damage to foreign by contacting infected cell, mutant, and transplanted cells and take several days to develop into an active cytotoxic T cell to destroy • T cells destroy by secreting molecules that form pores in target cells membrane than succumbs to lysis • Lysis- this is a process in which I fills with fluids and bursts MAST CELLS AND DENDRITIC CELLS • Precursors of mast and dendritic cells are formed in the bone marrow from hematopoietic stem cells. • Circulate freely and mature in the tissue. • Mast cells: found in skin and mucosal epithelial tissue; secrete histamine. • Dendritic cells: similar to macrophages in their ability to phagocytose or endocytose pathogens. LYMPHOID TISSUE • All leukocytes develop from hematopoietic cells (blood-forming) stem cells in the bone marrow. B • lymphocytes also fully mature in the bone marrow. T lymphocytes must migrate to the thymus gland before they develop into maturity. • Central lymphoid tissues: bone marrow and the thymus (as well as the fetal liver) are sites of lymphocyte maturation. • Peripheral lymphoid tissue: spleen, lymph nodes, tonsils, adenoids, appendix, lymph nodules (GI tract), and regions in the lining of the GI (Peyer’s patches); collections of B cells, T cells, and macrophages. • Each peripheral lymphoid tissues contains a dense network of cells hat trap microorganisms and foreign particles. • B ACTERIA :HAVE THEIR OWN DNA , THEIR MACHIENRY IS DIFFERENT WHILE THE CHEMICALS IN BACTERIA CAN INHIBIT THEIR ENZYMES WHILE ALLOWING OURS • V IRUSES-THEY ARE NOT CELLS • THEY MUST BE IN OUR CELLS TO USE OUR RIBOSOME P erih erallym pho idtisu e Spleen,mphnodes, tonsilsdenoids, appendi,andPeyer’s patches -Theseare collectionsofBcells, Tcellsnd m acrophes Figure23.1 LYMPHOCYTES REACH MATURITY IN CENTRAL LYMPHOID TISSUE AND INTERACT WITH FOREIGN ANTIGENS IN THE PERIPHERAL LYMPHOID TISSUE • THESE LYMPHOID TISSUES ARE INTERCONNECTED BY BLOOD VESSELS AND LYMPHOTIC VESSELS WHICH LYMPHOCYTES CIRCULATE Organizedstructureoflymphnode andspleen Lymphnode Spleen Figure24.2 Figure24.3 24.3 – the spleen has the same structure as the lymph node 24.2 – lymphotic vessels (green) – microforeign come inside . They can exist through the blood or vein • Spleen collects worn-out erythrocytes from the blood; it is also collecting bloodborne microorganisms and foreign particles. Microorganisms and particles carried in lymph are trapped by lymph node (where lymphatic vessels converge). • Macrophage and lymphocyte networks of the spleen and lymph nodes filter blood and lymph, respectively. • Tonsils and adenoids trap inhaled particles and microorganisms. • Appendix, lymph nodules and peyer’s patches trap substances that enter the body in ingested food or water. NONSPECIFIC DEFENSES Includes physical barriers, inflammation (a complex series of events causing accumulation of proteins, fluid, and phagocytic cells in an area of tissue that has been injured or invaded by microorganisms), interferons (a family of related proteins that can induce virus resistance to other cells),complement system ( a group of plasma proteins that act to lyse foreign cells). 1) physical barriers: • Skin and mucous membranes. • Skin consists of an outer epidermis and inner dermis. Epidermis consists of tightly packed epithelial cells and lacks blood vessels. • Outermost layer is composed of dead cells and keratin. • Within the dermis are sebaceous glands, which secrete an acidic oily substance, sebum that inhibits bacterial growth. • Viscous mucus, which bathes the surfaces of exposed epithelia and can trap foreign matter and potential pathogens. Have ciliated epithelial cells that line the trachea 2) INFLAMMATION • Microbial invasion or damage to tissue triggers a complex series of events that rapidly lead to inflammation of the affected tissue. • 5 major events: 1) nearby macrophages engulf debris and foreign matter 2) nearby capillaries dilate and become more permeable to proteins and fluid 3) foreign matter is contained 4) addition leukocytes migrate into the region 5) recruited leukocytes continue to help clear the infection, mainly by phagocytosis. Majorstepsoflocalinflammation Major Inflammation in detail steps: • Macrophages detect bacteria using receptor proteins. The resulting attachment initiates phagocytosis. • Also stimulates the macrophages to secrete cytokines, proteins that are secreted by cells in response to a stimulus. • Cytokines secreted by macrophages contribute to subsequent steps in inflammation. PERMEABILITY OF CAPILLARIES: • Nearby blood vessels dilate. The capillary walls become more permeable. • Increased blood flow brings additional leukocytes and defensive proteins into the local circulation. • Increased permeability allows these proteins to move into the tissues. • Leukocytes that gather in these dilated vessels migrate from the blood into the tissue spaces. • Vasodilation and increase capillary permeability are induced by histamine released from a variety of cells in response to injury. • Histamine 4 characteristic symptoms: redness, swelling, heat, and pain. As the capillaries become engorged with blood, the resulting increase in hydrostatic pressure plus the increased interstitial osmotic pressure that accompanies the leakage of plasma proteins causes fluid to filter out of the capillaries and into the tissue spaces, resulting in edema • The edema exerts pressure against the surrounding tissue and skin, which
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