Untitled Quiz

Primary response: first exposure to an antigen, naive B cells are activated to proliferate and differentiate into plasma cells and memory cells
Secondary response: subsequent exposures to the same antigen, memory B cells are activated to produce larger amounts of antibodies with more heavy-chain class switching and affinity maturation.

Signals generated during innate immune responses cooperate with antigen recognition by B cell receptors.
Complement activation leads to the binding of C3d to microbes. B cells recognize both the microbial antigen and bound C3d through CR2.
Microbial-derived PAMPs can activate Toll-like receptors (TLRs) on B cells at the same time as antigen recognition.

Multivalent antigen activation initiates B cell proliferation and differentiation, preparing them for interaction with helper T cells.
Antigen activation in lymphoid organs initiates B cell proliferation, IgM secretion, and prepares B cells for helper T cell interaction.

T and B lymphocytes independently recognize antigens in peripheral lymphoid organs and are activated.
Activated cells migrate towards one another and interact at the edges of lymphoid follicles.
Plasma cells are initially produced in extrafollicular foci where activated T and B cells interact.
Some activated B and T cells migrate back into the follicle, forming germinal centers where the antibody response fully develops.

Early T-dependent humoral response occurs in extrafollicular foci, generating low levels of antibodies with limited isotype switching.
Activated B cells induce further T cell activation and their differentiation into Tfh cells.
Activated B cells and Tfh cells migrate into follicles and form germinal centers.
Full T-dependent humoral response develops in germinal centers, leading to:
- Extensive isotype switching and affinity maturation
- Generation of long-lived plasma cells
- Development of long-lived memory B cells

B cells specific for a protein antigen bind, internalize, and process the antigen.
They present peptides attached to MHC class II molecules to helper T cells.
Both B cells and helper T cells are specific for the same antigen, but B cells recognize native epitopes, whereas helper T cells recognize peptide fragments of the antigen bound to MHC class II molecules.

Helper T cells recognize peptide antigens presented by B cells on MHC class II molecules.
Activated helper T cells express CD40L and secrete cytokines, which bind to receptors on the same B cells, activating them.

Protein antigen binding to naive B cell Ig receptors initiates T-dependent responses in lymphoid follicles.
The B cells internalize and process antigen, presenting MHC class II displayed peptides to activated helper T cells.
These helper T cells contribute to early B cell activation in extrafollicular sites.

IgA: main function is to bind antigens on microbes before they invade tissues, first defense for mucosal surfaces.
IgD: present on the surface of B cells and involved in the induction of antibody production.
IgM: involved in the ABO blood group antigens on red blood cells, enhances cell ingestion by phagocytosis, primary response.
IgG: provides long-term protection, persists for months and years, protects against bacteria and viruses, neutralizes bacterial toxins, triggers complement protein systems, and enhances phagocytosis by binding antigens.
IgE: binds to mast cells and basophils, plays a role in parasitic infections and allergic reactions.

Antibodies coat microbes, promoting their ingestion by phagocytes.
IgG subclasses bind to microbes and are recognized by Fc receptors on phagocytes.
Fc receptor signals promote phagocytosis and activation of phagocytes to destroy microbes.

Certain IgG antibodies bind to antigens on infected cell surfaces, and their Fc regions are recognized by Fc receptors on NK cells.
NK cells kill antibody-coated cells.

Three major pathways: alternative, lectin, and classical.
Alternative and lectin pathways are initiated by microbes in the absence of antibody.
Classical pathway is initiated by antibody binding to antigens.

IgM or IgG binding to antigens triggers the pathway.
Adjacent Fc regions of antibodies bind to C1 complement protein.
C1 becomes enzymatically active, cleaving C4 and C2.
C4b binds to the antibody and then binds C2, forming the C4b2a complex (classical pathway C3 convertase).
The C3 convertase cleaves C3; C3b binds to the complex forming C4b2a3b (C5 convertase).
C5 convertase cleaves C5.

IgA: produced in mucosal lymphoid tissues, transported across epithelia, and neutralizes microbes in mucosal lumens.
In the gastrointestinal and respiratory tracts, IgA is produced by plasma cells in the lamina propria and transported through epithelial cells by the poly-Ig receptor.
On the luminal surface, IgA binds to ingested or inhaled microbes, blocking their entry through the epithelium.

Many bacteria and viruses mutate their antigenic surface molecules to evade antibody recognition.
HIV mutates its genome at a high rate, changing its surface antigen gp120. Antibodies against one subtype may not protect against others.
Bacteria like E. coli vary antigens in their pili to evade antibody-mediated defense.
Trypanosomes express new surface glycoproteins when encountering antibodies against the original glycoprotein.
Microbes can inhibit complement activation, resist opsonization, and phagocytosis by concealing surface antigens.

Naive B lymphocytes recognize antigens and differentiate into antibody-secreting plasma cells under the influence of helper T cells and other stimuli.

7Humoral immunity is mediated by antibodies.
Antibodies prevent infections by blocking microbial entry and eliminating microbes through effector mechanisms.
Antigen-binding (Fab) regions are spatially separated from effector (Fc) regions in antibody molecules.
Antibody neutralization of microbes and toxins depends solely on the antigen-binding regions.
Fc-dependent effector functions are activated only after antibodies bind antigens.
Antibodies neutralize microbes and toxins by interfering with their attachment to host cells.
Antibodies coat (opsonize) microbes, promoting phagocytosis by binding to Fc receptors on phagocytes.