Whilst there is some overlap between these arms of the immune response - both rely on the functions of lymphoid cells - there are also some important differences. One can acquire humoral immunity to a specific infection or disease if administered with antibodies from someone who was previously been exposed to the same infection, circumventing the humoral response. However, antibody-mediated immunity involves a set of molecular components and processes that differ from cell-mediated immunity.
In this article, we define humoral immunity and cell-mediated immunity, discussing the different immune processes, purposes and important cell types. These lymphocytes express a variety of antigen-specific molecules that are essential for the detection of infectious agents in the human body.
With the help of T cell lymphocytes, in turn activated by MHC class II receptors that recognize microbial-associated antigens, the activated memory B cells express these antigen-specific molecules on their surface while the effector B cells secrete these molecules in the blood to bind the antigen of interest. Antibodies neutralize antigens primarily through mechanisms of attachment and accumulation.
Antibodies can also participate in processes that lead to the lysis or killing of infected or antigen-presenting cells through the activation of the complement cascade or interaction with effector cells and release of cytokines. With assistance from helper T cells, B cells will differentiate into plasma B cells that can produce antibodies against a specific antigen.
The humoral immune system deals with antigens from pathogens that are freely circulating, or outside the infected cells. Antibodies produced by the B cells will bind to antigens, neutralizing them, or causing lysis dissolution or destruction of cells by a lysin or phagocytosis.
Cellular immunity occurs inside infected cells and is mediated by T lymphocytes. The pathogen's antigens are expressed on the cell surface or on an antigen-presenting cell. The infected cell then undergoes lysis. Tell us what you think about Healio. Begin your journey with Learn Immuno-Oncology. Once activated, the B cell proliferates and differentiates into antibody-secreting plasma cells.
Figure 3. Click for a larger image. In T cell-dependent activation of B cells, the B cell recognizes and internalizes an antigen and presents it to a helper T cell that is specific to the same antigen. The helper T cell interacts with the antigen presented by the B cell, which activates the T cell and stimulates the release of cytokines that then activate the B cell.
Activation of the B cell triggers proliferation and differentiation into B cells and plasma cells. T cell-dependent activation of B cells is more complex than T cell-independent activation, but the resulting immune response is stronger and develops memory. T cell-dependent activation can occur either in response to free protein antigens or to protein antigens associated with an intact pathogen. The presented antigen is then recognized by helper T cells specific to the same antigen.
The coordination between B cells and helper T cells that are specific to the same antigen is referred to as linked recognition. Once activated by linked recognition, T H 2 cells produce and secrete cytokines that activate the B cell and cause proliferation into clonal daughter cells.
After several rounds of proliferation, additional cytokines provided by the T H 2 cells stimulate the differentiation of activated B cell clones into memory B cells , which will quickly respond to subsequent exposures to the same protein epitope, and plasma cells that lose their membrane BCRs and initially secrete pentameric IgM Figure 3.
This process, called class switching or isotype switching , allows plasma cells cloned from the same activated B cell to produce a variety of antibody classes with the same epitope specificity. The variable region is not changed, so the new class of antibody retains the original epitope specificity.
T cell-dependent activation of B cells plays an important role in both the primary and secondary responses associated with adaptive immunity. With the first exposure to a protein antigen, a T cell-dependent primary antibody response occurs. The initial stage of the primary response is a lag period , or latent period , of approximately 10 days, during which no antibody can be detected in serum.
The end of the lag period is characterized by a rise in IgM levels in the serum, as T H 2 cells stimulate B cell differentiation into plasma cells. IgM levels reach their peak around 14 days after primary antigen exposure; at about this same time, T H 2 stimulates antibody class switching, and IgM levels in serum begin to decline. Meanwhile, levels of IgG increase until they reach a peak about three weeks into the primary response Figure 4.
During the primary response, some of the cloned B cells are differentiated into memory B cells programmed to respond to subsequent exposures. This secondary response occurs more quickly and forcefully than the primary response.
The lag period is decreased to only a few days and the production of IgG is significantly higher than observed for the primary response Figure 4. In addition, the antibodies produced during the secondary response are more effective and bind with higher affinity to the targeted epitopes. Plasma cells produced during secondary responses live longer than those produced during the primary response, so levels of specific antibody remain elevated for a longer period of time.
Figure 4. Compared to the primary response, the secondary antibody response occurs more quickly and produces antibody levels that are higher and more sustained.
The secondary response mostly involves IgG. T-independent antigens can stimulate B cells to become activated and secrete antibodies without assistance from helper T cells. A patient lacks the ability to make functioning T cells because of a genetic disorder. Explain your answer. Skip to main content.
0コメント