vocab  Tonsillitis  Mucosa-associated lymphatic tissue (MALT)  Pathogen  Complement fixation  Pyrogens  Chemotaxis  Immunocompetant  Autograft  Isograft  Allograft  Xenograft  Hapten  Allergy/hypersensitiviy  Immediate/acute hypersensitivity  Anaphylactic shock  Delayed hypersensitivity  Immunodeficiency  Severe combined immunodeficiency disease  Acquired immune deficiency syndrome  Autoimmune diseases  Multiple sclerosis  Myasthenia gravis  Graves’ disease  Type 1 diabeties  Systemic lupus erythematosus  Glomerulonephritis  Rheumatoid arthritis

Lymphatic and Immune System

Inflammatory response  Blood vessels dilate creating the heat and redness and directing more blood to the area.  Within the first hour neutrophils move out of the capillaries to the injured tissue and begin engulfing damaged/dead cells and pathogens.  Monocytes that follow the neutrophils begin as poor phagocytes but after 8-12 hrs they become macrophages and replace the short lived neutrophils.  This process occurs concurrently with the blood clotting process discussed in the previous unit.  If pathogens have invaded the tissues the third line of defense is the immune response.

Specific body defense  Aka immune response aka third line of defense attacks particular foreign substances.  Recognizes foreign molecules (antigens) and acts to inactivate or destroy them.  3 important aspects of immunity:  It recognizes and acts against particular pathogens and foreign substances  It is not restricted to the initial infection site  The initial exposure to an antigen “primes” the body or creates a “memory” to react more vigorously next time.  There are two overlapping branches of immunity. Humoral immunity is based on antibodies located in the “humors” or fluids. Cellular immunity where living cells attack cells either directly by lysing them or indirectly by releasing chemicals.

Structures involved in specific body defenses  Antigen: any substance capable of exciting our immune system and creating an immune response. All types of macromolecules can act as antigens but proteins are the strongest. Our cells have antigens but as the immune system develops it takes an inventory of the “self-antigens” so it can identify the nonself antigens. However, a person’s “self-antigens” would be foreign if placed in another person’s body.

 T Lymphocytes: do not produce antibodies. Involved in cell mediated immunity. Arise from lymphocytes that migrate to the thymus and mature in 2-3 days. Their maturation is controlled by the hormones of the thymus like thymosin. These cells divide rapidly but only the ones best able to identify foreign antigens and ignore self antigens survive. Structures involved in specific body defenses

 B Lymphocytes: produce antibodies and supervise humoral immunity. These cells develop fully in the bone marrow. Both type of WBCs become immunocompetent (able to identify and fight one particular antigen) as they mature before they are released to fight infection. This means that our genes determine our immunity. After fully developing both T and B cells migrate to the spleen and lymph nodes and circulate throughout the body where they will meet the antigen they are specific to. When they bind with the foreign antigen their differentiation is complete. Structures involved in specific body defenses

 Macrophages: arise from monocytes in the bone marrow and migrate to lymph organs where they remain. These cells engulf foreign particles and present fragments of the antigens on their own surface as red flags for T cells. They also secrete proteins called monokines that are important to the immune response. T cells can release chemicals which make macrophages even more active to speed up the immune process. Structures involved in specific body defenses

Humoral immune response:  An immunocompetent B cell will not reach full maturity until an antigen binds to its surface receptors to “sensitize or activate” it.  The B cell then undergoes clonal selection where is grows and multiplies rapidly creating exact replicas of itself or clones. This process is the primary humoral response.  These clones will mostly become plasma cells that are antibody producing factories producing 2000 antibodies per second. This activity will last 4-5 days and then the plasma cells begin to die. The antibody levels in the blood peak about day 10 and then slowly decline.

Humoral immune response:  The clones that don’t become plasma cells develop into long- lived memory cells which will respond to the antigen if it ever enters the body again.  This interaction would be secondary response which is much faster and more prolonged and effective. Within hours of the antigen entering the body new plasma cells are made and in 2-3 days antibody levels in the blood peak and remain high for weeks to months.

Humoral immune response:  Antibodies/immunoglobulins (Igs) are soluble blood proteins that bind with a specific antigen. Their basic structure includes  Heavy chain: longer amino acid chains that are identical to each other  Light chain: shorter amino acid chains that are identical to each other  Disulfide bonds: connect the four amino acid chains together into a T or Y shape  Variable region: region of amino acid chain that is different between antibodies, variable region of the light and heavy chain combine to form an antigen-binding site to “fit” the antigen  Constant region: form the stem of the antibody  There are five basic classifications based on the antibodies structure and function (MADGE).

Humoral immune response:  Active humoral immunity: when your B cells encounter an antigen and create antibodies against them. Naturally acquired immunity occurs when an active pathogen enters the body prompting the humoral response. Artificial acquired immunity occurs when a vaccine containing dead or attenuated pathogens is used to prompt a response. Regardless the response from the body is the same.

Humoral immune response:  Passive humoral immunity: when antibodies are removed from a donor and placed into your body. This means your B cells are not challenged by the antigen and will not create immunological memory. The protection of these antibodies ends as they are naturally degraded and removed. This occurs naturally when antibodies are passed from mother to fetus through the placenta. This can be artificially performed when a person receives immune serum or gamma globulin after an exposure. These include hepatitis, antivenum for snake bites, botulism, rabies, and tetanus. These things would normally kill a person before active immunity could be established so the antibodies offer immediate protection for 2-3 weeks.

Cellular Immune Response:  Macrophages must engulf foreign antigens, digest them, and present pieces of them along with pieces of self- proteins in order for a T cell to recognize the antigen and bind with it.  At this point the T cell becomes fully mature and activated to make clones.  Cytotoxic (killer) T cells bind with virus infected, cancerous, or foreign graft cells and injects a toxin called perforin which causes the cell to ruptures.

Cellular Immune Response:  Helper T cells circulate throughout the body recruiting other cells to fight invaders such as interacting with activated B cells and encouraging them to divide faster and signaling for antibody creation to begin.  Helper T cells also release cytokine chemicals called lymphokines that stimulate killer T and B cells, attract other WBCs to the area and stimulate macrophages to become even more phagocytic.

Cellular Immune Response:  Suppressor T cells suppress the activity of T and B cells once and antigen has been destroyed to prevent unnecessary immune system activity. Memory T cells remain to provide immunity to the antigens in the future.