Animal Immune Systen

Updated 2007-05-23 23:01
Innate immunity-non-specific to any pathogen which consists of inflammation. Barriers, leukocytes and fever (first response)
Acquired (adaptive) immunity-specific:attacts specific pathogens and consists of humeral and cell-mediated immunity
Humoral immunity-helper t-cells make B lymphocytes that make antibodies to attack cells displaying certain antigens
Cell-mediated immunity-T lymphocytes attack cells displaying certain antigens
Skin-has psoriacin which kills bacteria and keeps water in and pathogens away from body
Eyes-have lysozyme which causes bacteria to explode
Ears-have hair and wax
Nose-has hair and mucous to trap invading pathogens
Digestive tract- saliva has lysozyme as well and stomach acid which kills bacteria
Airways-have cilia and mucous
What activates the inflammatory response? Leukocytes
Inflammatory response-swelling and redness and
1.plateletsstimulate scab
2.mast cells-activates after getting a cut and releases histamine causing dilation of vessels leading to the wound and constricting those leading away to wound so white blood cells can get to the site
3. Neutrophiles- chemotaxis…secrete factors that kill pathogens and remove bacteria with phagocytes
4. Macrophages-secrete cytokines which attract immune system cells to the site and activate tissue repair also uses phagocytes
Immunological “memory”- in the acquired immune response which produces antibodies preventing re-infection
Lymphocytes-attack specific pathogens and create memory
What makes B cells? Bone marrow
What makes T cells?Thymus
What happens to lymphocytes upon exposure to a pathogen? Rough ER makes proteins to kill pathogens and spleen and lymph nodes are activated
Antigen-made by lymphocytes and are flags which are chemicals that stick out of cell
Self-antigens- all cells have so they aren’t attacked (only attack foreign antigens)
What do lymphocytes have that binds to antigens and marks them for destruction?Receptors
Why is it that lymphocytes can bind to an endless diversity of antigens?Because their receptors undergo genetic recombination
Autoimmune disease-lymphocytes bind to self-antigens
What is the first step in T-cell activation? Ingestion and presentation of antigens by dendric cells then the antigens combine with MHC protein in ER and the complex presents itself to the surface.
When a T-cell (CD4+t-cells) binds to an antigen what is activated? Clonal expansion where t-cells multiply and differentiate into 2 types of effector t-cells
What are the 2 types of effector t-cells that are generated in clonal expansion? cytotoxic t-cells which attack the virus-infected cells (cell-mediated immunity) and helper t-cells which activate B cells (humoral immunity)
B cell activation(humoral)- b cell eats antigen and externalizes it with MHC, then helper t-cells bind to that same antigen activating the b cell. Clonal expansion happens and b cells clone into plasma cells which secrete antibodies.
Cell-mediated response-CTL (cytotoxic t-lymphocyte) makes contact with virus-infected cell and releases granules which induce cell to self-destruct
Humoral response-antibodies coat free virus particles so the particles cant fuse with the host cell’s plamsa membrane then the antibody-coated virus is recognized by macrophage and phagocytosed
Is the initial or second immune response quicker? Second because of memory and more antibodies
How do vaccines work?They contain viral epitopes or weakened viruses to build memory and protect body against further infections
HIV-kills helper t-cells and macrophages
AIDS-an acquired immune deficiency when helper t-cell count gets super low
Why is it so hard to find an effective vaccine for HIV? It mutates quickly