8.1 Humoral Immunity

The primary defense mechanism used to combat microbes in the lumens of mucosal organs and in newborn fetus. These are proteins that specifically bind to antigens.

Antibodies against microbes and microbial toxins bind to these receptors and prevent their attachment to cells.

This receptor plays a critical role in the immune response to parasitic worms by mediating IgE-dependent cytotoxicity.

Antibodies initiate a cascade of events leading to the lysis of pathogens. This molecule triggers the classical pathway of complement activation by binding to the antibody-antigen complex.

This immune mechanism relies on NK cell receptors that bind to antibodies attached to target cells, leading to the destruction of the target cell.

This coreceptor on B cells facilitates the activation of B cells by binding to complement components bound to antigens.

Along with the CR2 coreceptor, the engagement of these receptors by microbial products further enhances B cell activation. These receptors act as sensors for microbial features.

When the BCR binds to antigens, it internalizes them into endosomal vesicles, where antigens are processed into peptides that are presented by class II MHC molecules.

These receptors on B cells are engaged by microbial products to enhance B cell activation, serving as a second signal for B cell activation.

Immune responses are initiated by the recognition of specific antigens by T cells and B cells. This is the first step in mounting an immune response.

This is the area where activated lymphocytes interact during T cell-dependent antibody responses. Interactions lead to the development of antibody response.

These antigens contribute to the production of natural antibodies without requiring prior exposure to pathogens. These antibodies provide a first line of defense.

This negative feedback mechanism involves the formation of immune complexes that bind to inhibitory Fc receptors on B cells, effectively dampening the antibody response.

Secreted IgG antibodies bind to these inhibitory Fc receptors on B cells, inhibiting further B cell activation. This prevents excessive antibody production.

This cytoplasmic tail of FcγRIIB is involved in negative signaling, inhibiting the activation of B cells. This acts as a regulator of B cell activation.

Activated Th cells engage with B cells through this receptor to promote their proliferation and differentiation. This interaction is crucial for humoral immunity.

Activated Th cells play a crucial role in humoral immune responses by secreting cytokines that bind to receptors on B cells, driving their differentiation into antibody-producing plasma cells.

This type of antibody is a major player in mucosal immunity, preventing microbes from entering through the epithelium.

CD40 signals are essential for isotype switching, ensuring that the appropriate antibody isotype is produced for the specific antigen.

This enzyme is crucial for isotype switching, allowing B cells to produce different antibody classes with distinct effector functions.

This process involves mutations in the antibody genes, leading to the production of antibodies with increasing affinity for the specific antigen. This fine-tunes the antibody response.

This type of antibody is involved in the elimination of helminths and allergic reactions. This antibody plays a role in parasite defense and allergy.

This process involves cutting and recombining the Ig heavy chain DNA in B cells, allowing for the production of different antibody classes with distinct functions.

This immune response involves the activation of naive B cells resulting in the production of antibodies with lower affinity and is slower developing. It's the initial response to an antigen.

Follicular B cells (B2 cells) are specialized in responding to protein antigens. These cells contribute to the adaptive immune response against protein-based pathogens.

Marginal zone B cells are a unique subset of B cells that recognize multivalent antigens like polysaccharides. These cells play a significant role in recognizing bloodborne pathogens.

The main difference between primary and secondary responses lies in the activation of B cells. Primary responses involve naive B cells, while secondary responses involve memory B cells, resulting in a faster and stronger response.

This antibody isotype is predominantly produced in T-independent responses. These responses are quicker but often provide short-lived protection.

This immune response occurs when B cells are specifically activated by antigens without the need for T cell help. This response is generally faster, but produces antibodies with lower affinity.

Naive B cells are lymphocytes that have not yet encountered antigens. They are found in secondary lymphoid organs and ready to respond to new pathogens.

This is the area within secondary lymphoid organs where activated helper T cells and activated B cells interact to initiate humoral immune responses. This is a crucial site for antibody generation.

Helper T cells recognize antigens presented by MHC-peptide complexes on B cells. This interaction leads to the activation of B cells and the production of antibodies.

Activated B cells proliferate rapidly in the extrafollicular foci. This response is important for controlling the spread of infection and generating a rapid antibody response.

Germinal centers form within follicles during T cell-dependent antibody responses to protein antigens. These centers are important for affinity maturation and the generation of memory B cells.

Naive CD4+ T cells are naive helper T cells that haven't encountered their specific antigens yet. They are crucial for the activation of the adaptive immune system.

B cell activation in response to protein antigens initially occurs in extrafollicular foci. This generates a quick response to the antigen, but the antibodies produced may have low affinity.

CD40L interacts with this receptor on B cells, inducing their proliferation and differentiation into antibody-producing cells. This interaction is essential for T cell-dependent B cell activation.

The formation of extrafollicular foci in the spleen during T-dependent B cell activation helps to quickly control the spread of infection before a more comprehensive immune response develops.

Extrafollicular foci develop in the T cell-rich PALS (periarteriolar lymphoid sheath) of the spleen. This is a strategic location for rapid B cell activation in response to bloodborne antigens.

B cells are responsible for generating antibody-secreting plasma cells in the extrafollicular foci. These plasma cells produce a quick burst of antibodies to limit the spread of infection.

The antibodies generated in the extrafollicular foci are often characterized by low affinity. Although quickly produced, these antibodies may have weaker binding to antigens.

Plasmablasts, formed in germinal centers, ultimately migrate to the bone marrow. This is where long-lived plasma cells reside and produce antibodies for long-term immunity.

The bone marrow is the major site of long-lived plasma cell differentiation. This is where antibodies are produced for long-term protection against recurrent infections.

As B cells differentiate into antibody-secreting plasma cells, they undergo significant structural alterations including increased protein synthesis, especially of immunoglobulins, and a change in cell size for enhanced antibody production.

Mature plasma cells primarily secrete antibodies into the blood circulation. From there, antibodies can reach various tissues and organs to combat infection.

The differentiation of B cells into plasma cells results in a dramatic increase in cell size, reflecting the heightened antibody production capacity of the mature plasma cell.

Long-lived plasma cells play a vital role in providing long-term protection against recurrent infections. These cells constantly produce antibodies, ensuring immediate protection upon re-exposure to the same pathogen.

This process involves the selection of B cells producing antibodies with increasing affinity for the antigen. This results in a gradual increase in the affinity of the overall antibody response.

Helper T cells are essential in stimulating T-dependent antibody responses, particularly against protein antigens. This interaction allows for the generation of high-affinity antibodies and memory B cells.

These antigens can activate B cells without T cell help. They often contain repeating determinants, like polysaccharides, and are less effective at generating long-lasting immunity.