Immunity:The state of being resistant to injury, particularly by poisons, foreign proteins, and invading pathogens. Susceptibility: the lack of resistance to injury, foreign proteins and invading pathogens Innate immunity includes external physical and chemical barriers (skin and mucous membranes) and various internal defenses (phagocytes, natural killer cells, antimicrobial proteins); It does not involve specific recognition of a microbe, acts against all microbes in the same way; designed to prevent microbes from gaining access into the body and to help eliminate those that do gain access.Adaptive immunity: Involves the production of a specific lymphocyte or antibody against a specific antigen Innate Immunity First Line of Defense: Skin and mucous membranes.
Skin provides a barrier (epidermis); mucous membranes trap microbes and foreign substances and either eject them out of the body or sends them to an organ where they are destroyed. Innate immunity Second Line of Defense: Internal – antimicrobial proteins, natural killer cells and phagocytes 5 Steps of phagocytosis:1. Chomtaxis: a chemical attraction of phagocytes to a site of damage. Example: an invading microbe or damaged tissue cell might release chemicals that attract phagocytes.
2. Adherence: attachment of the phagocyte to the microbe or other foreign material.3. Ingestion: the plasma membrane of the phagocyte extends projections called pseudopods that engulf the microbe. Pseudopods fuse, surrounding the microorganism within a sac called a phagosome.
4. Digestion: the phagosome fuses with lysosomes to form a phagolysosome which breaks down the ingested cell. . Killing: the chemical onslaught by lysosomal enzymes. Any materials that cannot be digested further remain in structures called residual bodies.3 Stages of Inflammation:1.
Vasodilation and increased permeability of local blood vessels. Histamine is released causing vasodilation (increased diameter) of arterioles and increased permeability of capillaries, allowing more blood to flow and the removal of microbial toxins and dead cells.2. Emigration of phagocytosis. Within one hour after inflammatory response starts, hagocytes appear at site of injury. Neutrophils stick to inner surfaces of the blood vessels and begin to squeeze through the wall of the blood vessel, a process called emigration.
3. Chemostasis and microbial attack: neutrophils attempt to destroy invading microbes but they die off quickly; monocytes follow up and transform into wandering macrophages which also die. Within a few days the dead phagocytes and damaged tissue forms pus.4 Characteristics of Inflammation.In Cell Mediated Immunity, cytotoxic T cells directly attack target cells; it begins with activation of T cells by a specific antigen and ultimately results in elimination of the intruder; T Cell Receptors (TCRs) recognize and bind to antigen fragments; T cells undergo clonal selection then secrete cytokines like interleukin-2; Helper T cells display CD4 protein; cytotoxic T cells display CD8 protein and are activated by MHC molecules, then release granzymes which cause apoptosis; perforin causes cytolysis; and granulysin which enters the target cell to destroy microbes.
Antibody-mediated immunity – antibodies specifically target a particular antigen; begins when specific antigen binds to B cell receptors, activating B cells. They undergo clonal selection and form plasma cells; more intense process. Effector cells: carry out immune responses that ultimately destroy or inactivate the antigens. Most of these die after immune response is completed.
Memory cells: do not actively participate in the initial immune response to the antigen; but if the same antigen enter the body again in the future, memory cells are available to initiate a far swifter reaction than the first time; they respond by proliferating and differentiating into more effector cells and more memory cells; the second response is so fast and vigorous that the antigen is destroyed before any signs or symptoms of disease can occur. Plasma cells make antibodies against foreign intruders.
