B cells represent the second effector compartment of the adaptive immune response . Like T cells, each B cell expresses a unique anti gen receptor (B cell receptor: BCR), which consists of a membrane- bound copy of the antibody molecule that can be secreted by the B cell after activation [ 1 ]. In contrast to T cell receptors the BCR binds directly to molecular structures of pathogens with no need for previous antigen processing. Antigen binding by the appropriate BCR activates the B cell and induces proliferation and differentiation into plasma cells [ 2 ]. Plasma cells produce and secret large amounts of antibodies that are released in the blood and other body fluids. Antigen-specific antibodies are an important effector concept of additive immunity. Antibodies can facilitate phagocytosis or complement-mediated killing of pathogens or neutralize tox ins by binding to their appropriate antigens (Fig. 1 ).

Fig1. Antibody-mediated protection

Antibody molecules consist of a “constant” fragment (Fc fragment), a structural feature common to all antibodies of a given isotype, and a “variable” region, which includes the region that defines the antigen specificity (Fab fragment). The constant part of the molecule exists in five different classes (isotypes) termed immunoglobulin [Ig] A, IgD, IgE, IgG, and IgM. The Ig isotype deter mines the ability of an antibody class to localize to particular body sites and to recruit the optimal effector cells. The variable region of the antibody exists in a huge number of randomly generated different molecular configurations. This BCR repertoire guarantees maximal capability to recognize diverse pathogenic antigen. Activation of B cells after the first encounter with an antigen and subsequent differentiation into plasma cells usually needs 10–14 days. Initially plasma cells will typically produce IgM-type antibodies. IgM antibodies are large molecules consisting of five bivalent antibody molecules linked together to exhibit ten binding regions. In the further course of the immune response antibody production will switch to the IgG isotype, which also represents the major isotype of B cell memory responses [ 3 ]. Depending on the specific circumstances of B cell activation antibody production may switch to IgA which is secreted to mucus membranes or IgE, mainly for the defense of infections by parasites.

In most cases, optimal B cell activation and differentiation into antibody-secreting plasma cells will only be achieved when B and T cells are simultaneously activated by elements of the same pathogen (Fig. 2 ). T cell-independent direct activation of B cells occurs only in response to repetitive antigenic structures, such as carbohydrates found in bacterial walls. These T cell-independent immune response s are characterized by the secretion of low-affinity anti bodies of the IgM type, lacking the typical memory response upon reexposure to the same antigen.

Fig2. Immune response after vaccination. Adapted from Janeway et al. Immunobiology, the immune system in health and disease, 6th edition. New York: Garland Science Publishing 2005

In these instances, activated B cells will recruit the help of T cells to mount an optimal response and to elicit immunological memory. After activation of the B cell by binding to a pathogen antigen the surface BCR-antigen complex will be internalized and elements of the antigen are processed and presented to an appropriate CD4+ T helper cell. The interacting CD4+ T cell will differentiate into a follicular T helper cell in order to provide helper signals for the B cell. T cell-dependent B cell responses are characterized by the secretion of high-affinity antibodies and a large spectrum of isotypes (in particular IgG). The quality of antibody response has a bearing on protection, e.g., the antigen binding capability of antibodies (affinity, avidity) and the dynamics of the peak response (priming); long-term protection requires the persistence of antibodies and the generation of immune memory cells capable of rapid and effective reactivation [ 1 ].

References
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[1] Eibel H, Kraus H, Sic H et al (2014) B cell biology: an overview. Curr Allergy Asthma Rep 14:434

[2] Shapiro-Shelef M, Calame K (2005) Regulation of plasma-cell development. Nat Rev Immunol 5:230–242

[3] Deenick EK, Hasbold J, Hodgkin PD (2005) Decision criteria for resolving isotype switch ing confl icts by B cells. Eur J Immunol 35:2949–2955

مواضيع ذات صلة

الحساسية الدوائية نحو العوامل المخصرة للوصل العَصَبِي العَضَلِي

آليات حساسية السلفوناميدات ومظاهرها

Antigen - Antibody Interaction: Specificity and Cross - Reactivity

ANTIBODY SYNTHESIS

Tolerance to Commensal Microbes and Fetal Antigens

B Lymphocyte Tolerance

Peripheral T Lymphocyte Tolerance

Immune Memory

T Cells

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