Adaptive Immunity
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This is because the special properties of some bacterial polysaccharides, polymeric proteins, and lipopolysaccharides enable them to stimulate naive B cells in the absence of peptide-specific T-cell help. Unraveling Mechanisms and Discovering Novel Roles for Complement. B-Cells are the leukocytes that turn into plasma cells and release antibody once they have been activated.
Antibodies induced by microbial antigens alone are therefore less variable and less functionally versatile than those induced with T-cell help. The humoral immune response is initiated when B cells that bind antigen are signaled by helper T cells or by certain microbial antigens alone It is a general rule in adaptive immunity that naive -specific are difficult to activate by antigen alone.
T cell-dependent B cell activation. - Plasmablasts continue to divide rapidly but have begun to specialize to secrete at a high rate; they are destined to become nondividing, terminally differentiated plasma cells and thus represent an intermediate stage of differentiation.
Following maturation in the bone marrow and spleen, immunocompetent B cells remain in peripheral tissues until they encounter an antigen and are activated. B cell activation requires two distinct signals, and results in B cell differentiation into memory B cells or plasma cells. The first activation signal occurs upon antigen binding to B cell receptors BCRs. Upon binding to the BCR, the antigen is internalized by receptor-mediated endocytosis, digested, and complexed with MHC II molecules on the B cell surface. The second activation signal occurs via either a thymus-dependent or a thymus-independent mechanism. Most B cell responses to antigen require the interaction of B cells with T helper cells thymus-dependent activation. Presentation of an antigen-class II MHC complex on a B cell enables it to act as an antigen-presenting cell APC to T cells. T cell receptors TCR on T helper cells bind to the antigen-complexed class II MHC molecule on the B cell surface resulting in T cell activation. The activated T cell then provides a second activation signal to the B cell, which can occur through a variety of proteins. Alternatively, there are a few types of antigens that can directly provide the second B cell activation signal thymus-independent activation. These antigens include components of some bacterial cell wall components e. Upon activation, B cells proliferate and form germinal centers where they differentiate into memory B cells or plasma cells. Following differentiation into plasma cells, additional signals initiate plasma cell antibody class switching and regulate antibody secretion. The primary function of plasma cells is the secretion of B cell clone-specific antibodies. Each plasma cell secretes antibodies containing a clonally-unique antigen-binding region joined to a constant immunoglobulin Ig isotype-defining region.
The fact that both centroblasts and centrocytes proliferate and can express immunoglobulin explains how mutation and can take place simultaneously throughout the germinal center without the need for migration back and forth between the dark and light zones. Recent data suggest that the production of a spliced switch transcript has a role in directing switching, but the mechanism is not yet clear. Furthermore, this study showed that there is a similarity between B cell tumors and long-lived B cells in their signatures. An epitope on a viral coat protein is recognized by the surface immunoglobulin on a B cell and the virus is internalized and degraded. If the pathogen the cell can interact with is present the cell will be activated. Binding of CD40 by CD40L helps to drive the resting B cell into the cell cycle and is essential for B-cell responses to.
