| Question | Answer |
|---|
| 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.platelets | stimulate 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 |
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