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Lecture 32

MIMM 214 Lecture 32: Lymphocyte Development, Negative Regulation, and Immune Tolerance II
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Department
Microbiology and Immun (Sci)
Course
MIMM 214
Professor
Claire Trottier
Semester
Winter

Description
Lecture 32 (03.27) Monday, March 27, 2017 MEMORY AND VACCINES Protective Immunity • Second spike: early reinfection handled by preformed Abs/effector T cells from the previous response - not considered a memory response • Third spike: late (in years) reinfection handled by immune memory B/T cells o This is the memory response - a larger response as well Memory is the hallmark of adaptive immunity • Primary response is initiated upon first exposure to an antigen • Memory lymphocytes are left behind after antigen is cleared • A second exposure to the same antigen re-stimulates memory lymphocytes • Reactivation yields faster, more significant, better response o Doesn't come later after the innate, occurs at the same time o In the secondary response the innate response is not necessary for the adaptive response to occur (but there is still some innate activity) • Memory is NOT present in innate immunity Immunological Memory • Ability of the immune system to respond more rapidly and more effectively on a second encounter with an antigen o Dependent on adaptive immune mechanisms: • Ag-specific • Memory responses occur after primary response (secondary, tertiary, etc.) by lymphocytes initially generated late in the primary response • Long-lived • In practical terms, resistance to a particular infectious disease upon re-exposure to the microbe that causes that disease after having had that disease once before o Or after being vaccinated • The differences between primary and memory responses are: o More Abs, more cells o Different Abs, different lymphocyte features (higher affinity) The two main questions in the field of immunological memory are: • o What are the unique features of memory cells? o How is memory maintained? Features of Immunological Memory • Easier to detect/monitor for B cells than T cells • Mediated by a small and steady number of memory cells: o Some of the proliferating at a given time • Previous Ag exposure required • Long lived: o Abs: no significant decline after a while o T cells: gradual decrease (75 yrs?) B cell Memory 1. What are the key results following secondary exposure to the same antigen? a. More IgG in secondary response b. Faster onset of immune response c. Less IgM compared to primary response 2. What conclusions can you draw from this data? a. Higher affinity of antibodies in secondary response, faster because innate response isn't required to activate adaptive b. Memory B cells more responsible for secondary response - naïve B cells would secrete IgM Quantitative and Qualitative Differences in Memory Ab responses • Primary response: o Most IgM-producing cells come from primary focus o Some B cells will go to germinal centre where they will undergo somatic hypermutation and class switching late in the response • Secondary response: o Some memory B cells make IgM o Most memory B cells express IgG and will undergo further somatic hypermutation • Antibody affinity of IgG continues to increase Questions 1. Explain why antibodies are generated preferentially against the antigens that were found in the original strain of the virus a. The memory B cells produced from the original virus will dominate the subsequent immune response (as well as get "stronger" through somatic hypermutation)
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