Antibodies by B-cells

As described previously, the humoral immune response results in the proliferation, activation, and subsequent production of antibodies by B cells following antigenic exposure and stimulation. The functionality and interplay between the three primary types of immune cells (macrophage, B cells, and T cells) required to elicit a humoral response can be assessed through various in vitro assays using cells from the peripheral blood or lymphoid tissues. 

Activation is the term used to describe processes involved in the secretion of antibodies by B-cells and secretions of cytokines by T-cells, but it can also describe the process of proliferation of both types of cells. 

Two different immunodeficiency diseases are now known to result from defects in purine catabolic reactions. In adenosine deaminase deficiency, large concentrations of dATP inhibit ribonucleotide reductase. Consequently, DNA synthe- i= sis is depressed. For reasons that are not yet clear, this metabolic distortion is observed primarily in the T and B lymphocytes. ( / lymphocytes, or T cells, bear antibody-like molecules on their surfaces. They bind to and destroy foreign cells in a process referred to as cellular immunity. B lymphocytes, or B cells, produce antibodies that bind to foreign substances, thereby initiating their destruction by other immune system cells. The production of antibodies by B cells is referred to as the humoral immune response.) Children with adenosine deaminase deficiency usually die before the age of two because of massive infections. 

Antibodies secreted by B cells bind to foreign material (antigen) and serve as tags or identifiers for such material. Antibody-tagged bacteria. 

Idiotypic network. Idiotypic determinants (idiotypes) are unique antigenic epitopes characteristic of the antigen receptors on the surface of T and B cells. They are associated with the variable regions of these receptors. Antibodies produced by B cells as the result of antigenic stimulation can themselves stimulate the production of auto-anti-idiotypic antibodies which have the ability to combine with the B-cell receptor (Ig) and thus can dampen down the immune response. Idiotypes may likewise stimulate the production of T cells specific for idiotypic determinants. Jerne (1974) postulated his... 

AlQaoud, KM., Fleischer, B. and Hoerauf, A. (1998) The Xid defect imparts susceptibility to experimental murine filariasis - association with a lack of antibody and IL-10 production by B cells in response to phosphorylcholine. International Immunology 10, 17—25. 

B cells are produced by the bone marrow. In response to activation of CD4+ T helper cells (see below), B cells proliferate and produce antibodies. (The term CD stands for cluster of differentiation. They are proteins coating cell surfaces. Altogether, there are more than 160 different types of CDs.) The antibodies produced by B cells circulate in the bloodstream and bind to antigens. Once bound, other cells are in turn activated to destroy the antigens. 

Helper T-cell 2 Th2 CD4-H Coordination of immune response, particularly activation of antibody production by B-cells and responsible for switching class from IgM to IgE. 

Figure 31-1 (A) Locations of the primary and secondary tissues of the immune system. The primary lymphoid organs are the thymus, which makes T cells, and the hone marrow, which forms B cells. After moving from these organs into the blood circulation the cells reach one of the secondary lymphoid organs, which include lymph nodes, spleen, tonsils, and Peyer s patches on the small intestine. Immature dendritic cells are found in body tissues including skin and mucous membranes and respond to foreign proteins by inducing attack by T lyphocytes and antibody formation by B cells. (B) Schematic drawing of a lymph node. From Nossal.1 Courtesy of Gustav J. V. Nossal.

With one exception, all the mechanisms used by B cells to generate antibody diversity are also used by T cells to generate T-cell receptor diversity. The one mechanism that does not appear to operate in T-cell receptor diversification is somatic hypermutation. This is presumably because mutation would be likely to generate killer T cells that would wantonly attack self-molecules. This is much less of a problem for B cells, since most self-reactive B cells could not be activated without the aid of specific helper T cells. 

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