B Cell Receptor for Antigen
المؤلف:
Stefan Riedel, Jeffery A. Hobden, Steve Miller, Stephen A. Morse, Timothy A. Mietzner, Barbara Detrick, Thomas G. Mitchell, Judy A. Sakanari, Peter Hotez, Rojelio Mejia
المصدر:
Jawetz, Melnick, & Adelberg’s Medical Microbiology
الجزء والصفحة:
28e , p135
2025-07-15
519
B cells display a single homogenous clonal immunoglobulin molecule (~105 copies/cell) on their surface. These immunoglobulins serve as receptors (B-cell receptors [BCRs]) for a specific antigen, so that each B cell can respond to only one antigen or a closely related group of antigens. All immature B cells carry IgM immunoglobulin on their surface, and most also express IgD. Additionally, B cells have surface receptors for the Fc portion of immunoglobulins as well as for several complement components.
An antigen interacts with the B lymphocyte that shows the best “fit” by virtue of its immunoglobulin surface receptor. When antigen binds to this BCR, the B cell is stimulated to divide and form a clone (clonal selection). Such selected B cells proliferate and differentiate to become plasma cells that secrete antibody. Because each person can make approximately 1011 different antibody molecules, there is an antigen binding site on a B cell to fit almost any antigenic determinant.
The initial step in antibody formation begins with the binding of antigen to the surface immunoglobulin via the BCR. Then the following steps ensue: (1) The BCR with its bound antigen is internalized by the B cell and the antigen is degraded to yield peptides that are then returned to the cell surface bound to MHC class II molecules. (2) This MHC class II–peptide complex on B cells is recognized by antigen-specific helper (CD4) T cells. These T cells have already interacted with antigen-presenting dendritic cells and have differentiated in response to the same pathogen. This interaction can occur because the B cell and the T cell that have encountered antigen migrate toward the boundaries between B- and T-cell areas in the secondary lymphoid tissue. (3) Chemokines, such as CXCL13 and its receptor, CXCR5, play an important role in this migration process. (4) The CD40 ligand on T cells binds to CD40 on B cells, and the T cell produces IL-4, IL-5, and IL-6, which induce B-cell proliferation. (5) Finally, the activated B cells migrate into follicles and proliferate to form germinal centers; here somatic hypermutation and immunoglobulin class switching occur. Germinal center B cells that survive this process now differentiate into either anti body-producing plasma cells or memory B cells. Additional details on this topic can be found in the chapter reference, Murphy et al (2012).
It should be noted that some bacterial antigens can directly stimulate this antibody production and do not require T cell help to activate B cells. These antigens are usually bacterial polysaccharides and LPS. These thymus T-cell independent antigens induce B-cell responses with limited class switching and do not induce memory B cells. By passing T-cell participation can be an advantage for the host because an expedited immune response (IgM production) can be generated against selected organisms, such as, Haemophilus influenzae and Streptococcus pneumoniae.
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