Humoral Immune Response I

B lymphocytes are activated when they encounter a specific antigen.

Activated B cells multiply to increase their number.

Activated B cells become plasma cells that produce antibodies.

Some activated B cells become memory cells, providing long-term immunity.

The initial antibody response to an antigen.

B cell activation needing T helper cells for optimal antibody production.

B cell activation without T helper cells; less efficient antibody response.

B cells crucial for T-dependent responses; produce high-affinity antibodies.

Enhanced characteristics of antibodies produced during T-dependent responses.

B cells presenting antigens to T helper cells for activation.

Antigens processed and presented by B cells needing T-helper cell help.

Antigens activating B cells without T helper cells (T-independent).

Essential step in the T-dependent response where B cells receive help from T helper cells

B lymphocytes are primarily found in the cortex of a lymph node, specifically within structures called follicles.

T lymphocytes are located in the paracortex of a lymph node.

Dendritic cells capture antigens in epithelial surfaces, process them, and present them to T lymphocytes in the paracortex.

Activated B cells migrate from the follicle towards the paracortex to interact with T helper cells.

Activated T helper cells migrate from the paracortex towards the follicle to interact with B cells.

CCR5 is a chemokine receptor expressed by B lymphocytes, helping them stay in the B cell zone.

CCR7 is a chemokine receptor expressed by T lymphocytes, helping them stay in the T cell zone and guiding them towards the paracortex.

The process where B cells change the type of antibody they produce, from IgM/IgD to other isotypes like IgG, IgA, or IgE. This switch is triggered by signals from helper T cells and involves rearranging the DNA of the B cell.

Class switching is triggered by two main factors: 1) interaction between CD40 on B cells and CD40L on helper T cells, and 2) specific cytokines released by the helper T cells.

Cytokines, signaling molecules released by helper T cells, determine which antibody isotype B cells will produce. For example, IL-4 promotes IgE switching, while TGF-beta promotes IgA switching.

The process where B cells make antibodies with increasingly stronger binding to a specific antigen over time. This happens in germinal centers of lymph nodes as B cells are repeatedly exposed to the antigen.

Specialized B cells that 'remember' a specific antigen. They don't secrete antibodies immediately, but they can quickly respond if the antigen is encountered again, leading to a faster and stronger immune response.

Simultaneous engagement of the B cell receptor (BCR) with an antigen, the complement receptor 2 (CR2) with C3d, and the Toll-like receptor (TLR) with a PAMP (pathogen-associated molecular pattern) all contribute to enhanced activation of B cells.

Activated B cells start expressing proteins involved in cell survival and proliferation, antigen presentation (MHC molecules), cytokine receptors, CCR7 (a chemokine receptor), and immunoglobulin genes for antibody secretion.

C3d, a by-product of the complement system activation, binds to the complement receptor 2 (CR2) on B cells, enhancing their activation along with antigen binding to the B cell receptor.

Naive CD4+ T cells are activated in the T cell zone by dendritic cells presenting antigens. They differentiate into helper T cells.

Naive B cells are activated by antigens in the follicles of lymph nodes.

Activated B cells and T cells migrate towards each other and interact at the edges of the follicles, where the initial antibody response develops.

Some activated B cells migrate back into follicles to form germinal centers, where they undergo further differentiation and affinity maturation.

All the functional sequences (protein expression, proliferation, etc.) happen simultaneously upon antigen binding, not sequentially.

B cells found in the spleen's white pulp, mainly responding to blood-borne polysaccharides and lipids, particularly those from encapsulated bacteria like Streptococcus pneumoniae. They activate independently of T cells.

B cells residing in mucosal tissues (MALT) and the peritoneum, primarily responding to non-protein antigens. They initiate immune responses at the body's entry points.

The B cell receptor (BCR) complex, composed of membrane-bound immunoglobulin (IgM or IgD) and signaling proteins (Igα and Igβ), recognizes specific antigens. Its variable region allows for diverse antigen binding.

Non-protein antigens often have multiple identical epitopes, allowing them to bind to multiple BCRs simultaneously, triggering cross-linking. This signals B cell activation.

A receptor on B cells that binds to C3d, a fragment of the complement protein activated by the innate immune system. This interaction enhances B cell activation.

Receptors on B cells that recognize microbial products (PAMPs), triggering signals that boost B cell activation, proliferation, and antibody secretion.

Complement activation and microbial products directly activate B cells. This involves complement receptor 2 (CR2) binding to C3d and Toll-like receptors (TLRs) recognizing microbial products (PAMPs), leading to enhanced signals for B cell activation.

B cells can process and present antigens to T helper cells, assisting in their activation. This is crucial for the T-dependent B cell response, leading to the production of high-affinity antibodies.