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Chapter 10

Chapter 10.docx

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Department
Biology
Course Code
BIO120H1
Professor
Bebhinn Treanor

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Chapter 10  A successful primary immune response serves 3 purposes o Clears the infection o Temporarily strengthens defenses to prevent reinfection o Establishes long term immunological memory  Immunological memory ensures subsequent infections with same pathogen give faster, stronger secondary immune response o This memory response is produced by circulating antibody and by expanded clones of B cells and T ells formed during primary response  The purpose of vaccination is to produce a state of immunological memory against pathogen before the pathogen is encountered  Immune responses made in all secondary lymphoid tissues can terminate infection and give immunological memory  After termination of infection by primary immune response, elevated levels of high affinity pathogen-specific antibody is present in blood, lymph or mucosal surface o These levels sustained for months by plasma cells that replenish antibody that is used up or degraded o If pathogen reinvades during this period it will be coated by IgA or IgG or captured by IgE bound to mast cells and eosinophils. o Viruses are neutralized by antibody and will fail to infect cells, bacteria will be opsonized by antibody and complement and delivered for destruction to Fc receptors and complement receptors of phagocytes, parasites will be killed or ejected through mast cells and eosinophils activated by parasite specific IgE o Invading microorganisms are eliminated through combo of specific antibody and innate immunity o Pathogen gets no time to grow and replicate…so they don’t reach a level where lymphocytes are activated by antigen to give 2 immune response  Many infectious diseases are seasonal…more exposed in winter  Antibodies made against cold caught at the start of winter prevent reinfection with the same virus (protective immunity). A second cold during winter usually due to different cold virus. After first infection with cold virus, this residual antibody may be insufficient to stop reinfection by the same virus. Therefore, secondary immune response used (immunological memory)  Almost all plasma cells made in primary response live couple months. After they die, the amount of pathogen-specific antibody in the body declines through degradation. Most gone after 1 year.  After the level of pathogen specific antibody made during primary immune response declines, immune defense relaxed and potential for that pathogen to reestablish an infection increases o Seasonal disease-reinfection after 1 year from infection. Residual level of antibody + innate immunity, sufficient to prevent infection o If this doesn’t happen, pathogen grows, replicates and infection spreads to secondary lymphoid tissues=secondary immune response  During primary immune response, clonal expansion of pathogen specific T and B cells give rise to short lived effector cells (stop infection) and memory T cells and memory B cells (future protection)  In secondary immune response, these memory cells are activated by antigen to proliferate and differentiate into effector cells…increased speed and strength of secondary response vs primary…molecularly similar o Difference because memory cells are more sensitive to infection, more easily activated, more abundant than naïve lymphocytes specific for the same pathogen o Memory B cells go through isotype switching and affinity maturation so will produce more effective antibodies than IgM made at beginning of primary infection o Pathogen activated memory B cells go through more refinement through somatic hypermutation and affinity maturations of their immunoglobulins  Therefore, more memory B cells produced during secondary rd response and available for a future 3 response…each successive infection with pathogen further improves defenses of adaptive immunity  Immunological memory studied by Peter Panum o Ppl in Faroe islands infected by measles…60 years later when measles returned, ppl born after the first epidemic got the disease. Ppl who survived the first epidemic were resistant  Goal of vaccination is to immunize ppl with a benign form of pathogen and induce immunological memory so an infection with a pathogen will meet with a secondary immune response that terminates infection before causing disease...ex: smallpox  After vaccination, the level of vaccinia-specific antibody in the blood increases to max and over the next year decreases about 1% of the max. o Steady state maintained for 75 yrs o Vacinnia-virus used for vaccination o Maintenance of this level means that some plasma cells or effector B lymphoblasts must remain active in the production of vaccinia- specific antibody throughout life o After vaccination, virus-specific B cells in blood also increases to max level and declines over 10 yr period to reach stable level of 10% of max…maintained for life=memory B cells respond to smallpox or vaccination with vaccinia o Vaccination also causes formation of pools of CD4 T cells and CD8 T cells that persist for 75 yrs=respond to smallpox or vaccination with vaccinia  During primary infection, the proliferation and differentiation of antigen specific naïve B cells produce large numbers of antibody secreting plasma cells to confront infection, and smaller number of memory B cells for future infection  First antibodies made in primary response are low affinity IgM o Later, somatic hypermutation, affinity maturation and isotype switching give rise to high affinity IgG, IgA, IgE.  Memory B cells derived from clones of B cells making the highest affinity anitbodies o Weeks after primary infection cleared, memory B cells reaches max (sustained for life) o Second infection-100x more pathogen specific B cells respond  Memory B cells are more sensitive than naïve B cells to presence of specific antigen, respond quicker o Higher affinity of their antigen receptors make memory B cells more efficient n binding and internalizing antigen for processing and presentation to helper T cells o Memory B cells also have more MHC class II and co-stimulatory molecules on surface which makes their interaction with antigen specific helper T cells more efficient. 2 effects  Smaller pathogen population is sufficient to trigger a B cell response, which will therefore occur at earlier stage in infection than in pri
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