Ch. 7 Humoral Immune Response Practice Flashcards

Vocabulary flashcards covering the mechanisms of B lymphocyte activation, humoral immune responses, isotype switching, and affinity maturation based on lecture notes.

Humoral immunity

The arm of the adaptive immune response mediated by antibodies that functions to neutralize and eliminate extracellular microbes and microbial toxins.

B cell receptors (BCRs)

Surface-bound monomeric immunoglobulins, specifically $IgM$ and $IgD$, that recognize antigens and associate with $Ig\text{α}$ and $Ig\text{β}$ to transduce signals.

Heavy-chain isotype switching

The process by which progeny of a B cell clone begin to produce different antibody isotypes to mediate specialized effector functions; this process requires T cell help.

Affinity maturation

The process where the affinity of antibodies specific for microbial proteins increases over time during a humoral immune response, requiring T cell help and occurring in the germinal center.

T-dependent antigens

Protein antigens that require help from $CD4^{+}$ T cells to induce B cell proliferation, differentiation, heavy-chain class switching, and affinity maturation.

T-independent (TI) antigens

Nonprotein antigens, such as polysaccharides and lipids, which can activate B cells without T cell help by cross-linking multiple BCRs.

Follicular B cells

B cells that reside in and circulate through lymphoid follicles, primarily responding to T-dependent protein antigens with high-affinity antibody responses.

Marginal zone B cells

A subset of B cells that, along with B-1 cells, play a major role in antibody responses to T-independent antigens.

Primary antibody response

An antibody response to the first encounter with an antigen, typically producing low-affinity $IgM$ within 5-10 days.

Secondary antibody response

A rapid (1-3 days) and larger antibody response to subsequent exposures to a protein antigen, characterized by larger amounts of higher-affinity antibodies and heavy-chain class switching.

BCR co-receptor

A complex formed by $CR2$ ($CD21$), $CD81$, and $CD19$ that enhances B cell activation when $CR2$ binds to the complement fragment $C3d$.

$$C3d$$

A fragment derived from the degradation of $C3b$ that is deposited on the surface of a microbe and binds to complement receptor type 2 ($CR2$) as a second signal for B cell activation.

Extrafollicular focus

Also known as the primary focus, it is the area at the edges of lymphoid follicles where antigen-activated T and B cells first interact to produce short-lived plasma cells and low levels of antibody.

Germinal center

The site within lymphoid follicles, also called the secondary focus, where sustained B cell proliferation, differentiation, isotype switching, and affinity maturation occur.

T follicular helper (Tfh) cells

Specialized helper T cells expressing the chemokine receptor $CXCR5$ that migrate into B cell follicles to assist in the formation of germinal centers and the selection of high-affinity B cells.

Centroblasts

Rapidly proliferating B cells located in the dark zone of the germinal center that undergo extensive isotype switching and somatic mutation of Ig genes.

Centrocytes

B cells in the light zone of the germinal center that have high-affinity receptors and are selected by follicular dendritic cells (FDCs) to survive and differentiate.

Activation-induced deaminase (AID)

An enzyme induced in B cells by $Tfh$ cell signals that alters nucleotides in switch regions to facilitate switch recombination and somatic mutation.

X-linked hyper-$IgM$ syndrome

An immunodeficiency caused by a defect in the gene encoding $CD40L$ on the X chromosome, preventing B cell class switching and resulting in normal to high serum $IgM$ with little to no $IgG$, $IgE$, or $IgA$.

Neonatal Fc receptor (FcRn)

A specialized receptor expressed in the placenta and on endothelial cells that protects $IgG$ from catabolism, prolongs its half-life, and mediates the transfer of maternal $IgG$ to the fetus.

Antibody feedback

A mechanism to terminate humoral responses where secreted $IgG$ forms immune complexes that bind to the inhibitory receptor $Fc\text{γ}RIIB$ on naive B cells, blocking activating signals.

$$Fc\text{γ}RIIB$$

An inhibitory Fc receptor found on naive B cells containing an immunoreceptor tyrosine-based inhibition motif (ITIM) that terminates B cell activation upon binding antibody-antigen complexes.