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Antigen-specific memory T cells specific to viruses or other microbial molecules can be found in both central memory T cells (T CM) and effector memory T cells (T EM) subsets. . Although most information is currently based on observations in the cytotoxic T cells (CD8-positive) subset, similar populations appear to exist for both the helper T cells (CD4-positive) and the cytotoxic T ce
T-independent memory B cells. T-independent memory B cells are a subset called B1 cells. These cells generally reside in the peritoneal cavity. When reintroduced to antigen, some of these B1 cells can differentiate into memory B cells without interacting with a T cell. [4] These B cells produce IgM antibodies to help clear infection. [20]
These cells were named central memory T cells (T CM). They effectively stimulate dendritic cells, and after repeated stimulation they are able to differentiate in CCR7- effector memory T cells. Both populations of these memory cells originate from naive T cells and remain in the body for several years after initial immunization. [14]
When B cells and T cells are activated some become memory B cells and some memory T cells. Throughout the lifetime of an animal these memory cells form a database of effective B and T lymphocytes. Upon interaction with a previously encountered antigen, the appropriate memory cells are selected and activated.
When B cells and T cells are activated and begin to replicate, some of their offspring become long-lived memory cells. Throughout the lifetime of an animal, these memory cells remember each specific pathogen encountered and can mount a strong response if the pathogen is detected again.
Memory B cell activation begins with the detection and binding of their target antigen, which is shared by their parent B cell. [25] Some memory B cells can be activated without T cell help, such as certain virus-specific memory B cells, but others need T cell help. [26]
These daughter cells either become plasma cells or memory cells. The memory B cells remain inactive here; later, when these memory B cells encounter the same antigen due to reinfection, they divide and form plasma cells. On the other hand, the plasma cells produce a large number of antibodies which are released freely into the circulatory system.
T RM cells develop from circulating effector memory T cell precursors in response to antigen. The main role in formation of T RM cells has CD103 and expression of this integrin is dependent on the cytokine TGF-β. CD8 + effector T cells that lack TGF-β fail to upregulate CD103, and subsequently do not differentiate into T RM cells.