Kinetics of Antibody Formation and Immune Response Quiz

Kinetics of Antibody Formation and Immune Response

The immune response involves both innate and adaptive immune responses, coordinated by antigen presenting cells (APCs).
The three types of APCs are dendritic cells, macrophages, and B cells, which interact with antigens in unique ways.
APCs break down antigens into immunogenic epitopes, which can trigger adaptive immune responses.
T-dependent antigens are proteins, while T-independent antigens are polysaccharides, lipids, or nucleic acids.
The innate immune response does not have memory or kinetics, while the adaptive immune response does.
Memory is embedded within B and T cells, not within the antibody molecules themselves.
The fate of the immunogen involves equilibration, catabolic decay, and immune elimination phases.
The equilibration phase involves the diffusion of the antigen through the biological system.
The catabolic decay phase involves the breakdown of the immunogen, with little immunological response.
The immune elimination phase involves the rapid clearance of the circulating antigen, triggered by the adaptive immune response.
The kinetics of the immune response differ between the first exposure (primary response) and subsequent exposures (secondary response).
The primary response to T-dependent antigens involves a standard bell-shaped curve of antibody titer over time, while the secondary response involves a quicker onset of the immune elimination phase.Kinetics and Quality of Antibody Responses
Antibody responses to specific antigens follow a bell curve with a lag period, logarithmic growth, peak antibody production, and a decline phase.
The kinetics of the antibody response vary depending on the type of antigen and infectious disease, with some responses occurring in hours to days, while others can take months.
The lag period of the antibody response corresponds to the equilibration and catabolic decay phase of the antigens, while the logarithmic phase is the immune elimination phase.
The secondary immune response follows a bell curve as well, but with a shorter lag period, higher antibody titer production, and a protracted plateau phase.
The secondary immune response is dominated by memory cells, which produce predominantly IgG antibodies rather than IgM.
The primary immune response is dominated by IgM antibodies, with a smaller bump in IgG antibodies due to clonal selection and class switching.
Affinity maturation occurs during the secondary immune response, which results in tighter fitting antibodies to antigens due to somatic hypermutation in the germinal center of lymph nodes.
The affinity of IgM antibodies to antigens does not change significantly over subsequent exposures, as a separate population of IgM-producing B cells is always present.
The quality of antibody responses varies between primary and secondary immune responses, with the latter producing more specific and higher affinity antibodies.
The kinetics and quality of antibody responses are highly specific to the antigen and infectious disease being targeted.
Antibody responses can provide protection against subsequent exposures to the same antigen, with the secondary immune response providing a faster and more effective response due to memory cells.
Antibody responses are key in protecting against infectious diseases, and understanding the kinetics and quality of these responses is crucial in developing effective vaccines and treatments.Affinity Maturation, Cross-Reactivity, and Autoimmunity
There are two types of B cells: conventional B cells and CD5-positive B cells, also known as B1 cells.
CD5-positive B cells are more primitive and mainly produce IgM antibodies with a general affinity.
Conventional B cells produce antibodies of different classes and can undergo class switching.
Affinity of antibodies improves over time through affinity maturation, which is better in the secondary immune response than in the primary immune response.
Affinity is inversely related to the dose of antigen, with low doses leading to tighter binding affinities.
Autoimmune disorders can be triggered by infectious agents and are often due to cross-reactivity between antigens from the infectious agent and self-antigens.
Cross-reactive antigens have low affinity in the early stages of immune response but can lead to higher affinity antibodies in the presence of high antigen doses.
B cells are antigen-processing cells and become great APCs in low antigen concentrations.
Clonal selection and affinity maturation through somatic mutation are proven through experiments with B cells in petri dishes.
Autoimmune disorders are a type of hypersensitivity and can result from cross-reactivity between antigens of infectious agents and self-antigens.
Cross-reactivity can occur when antigens from infectious agents resemble self-antigens.
Affinity maturation improves antibody binding affinity over time and is inversely related to antigen dose.The Kinetics of Immune Responses to T-Dependent and T-Independent Antigens
Clonal selection occurs when a B cell recognizes an antigen and is activated to produce antibodies.
Affinity maturation and somatic hypermutation can occur in response to T-dependent antigens, leading to the production of cross-reactive antibodies.
Vaccines are given in small doses to avoid generating cross-reactive antibodies by accident.
Memory B cells are generated in the secondary response to T-dependent antigens.
T cells coordinate with B cells to provide permission to make antibodies and generate cytokines that drive immune reactions.
Memory T cells can provide long-term immunity, as seen in survivors of the Spanish flu and potentially in response to COVID-19.
T-independent antigens, such as polysaccharides, only generate IgM antibodies and do not undergo affinity maturation or class switching.
Thermodynamically conservative immune responses occur to conserve energy in response to lower-level immunological phenomena, such as the production of IgM antibodies to polysaccharides.
Molecular events in B cells, such as DNA rearrangement and transcription factor binding, lead to the production of different isotypes of antibodies.
The first antibody made in response to an antigen is typically IgM, but the same binding can be attached to different isotypes as the antibody titer switches.
Transcription factors bind to switch sites in the DNA to regulate the production of different isotypes of antibodies.
Cytokines drive the immune response to specific antigens, leading to the production of different isotypes of antibodies.