Immunological memory is the ability of the immune system to quickly and specifically recognize an antigen that the body has previously encountered and initiate a corresponding immune response. Generally, they are secondary, tertiary and other subsequent immune responses to the same antigen. The adaptive immune system and antigen-specific receptor (e.g., T-cell receptors) generation are responsible for adaptive immune memory. After the inflammatory immune response to danger-associated antigen, some of the antigen-specific T cells and B cells persist in the body and become long-living memory T and B cells. After a second encounter with the same antigen, they recognize the antigen and mount a faster and more robust response. Immunological memory is the basis of vaccination. Emerging resources show that even the innate immune system can initiate a more efficient immune response and pathogen elimination after the previous stimulation with a pathogen, respectively with pathogen-associated molecular patterns (PAMPs) or damage-associated molecular patterns (DAMPs). Innate immune memory (also called trained immunity) is neither antigen-specific nor dependent on gene rearrangement; the different response is caused by changes in epigenetic programming and shifts in immunometabolism. Innate immune memory has been observed in invertebrates and vertebrates. Immune memory can be lost if the corresponding memory cells die out ("immune amnesia"). For example, previously acquired immune memory can be depleted by measles in unvaccinated children, leaving them at risk of infection by other pathogens in the years after infection. This weakening of the immune system increases the risk of death from other diseases.
Adaptive immune memory
Immunological memory occurs after a primary immune response against the antigen. Immunological memory is thus created by each individual after a previous initial exposure to a potentially dangerous agent. The course of secondary immune response is similar to the primary immune response. After the memory B cell recognizes the antigen, it presents the peptide in the MHC class II complex to nearby effector T cells. That leads to activation of these cells and rapid proliferation of cells. After the primary immune response has disappeared, the effector cells of the immune response are eliminated. However, antibodies that were previously produced in the body persist and represent the humoral component of immunological memory and serve as an important defense against subsequent infections. In addition to the formed antibodies in the body, there remains a small number of memory T and B cells that make up the cellular component of the immunological memory. They stay in blood circulation in a resting state, and at the subsequent encounter with the same antigen, these cells are able to respond immediately and eliminate the antigen. Memory cells have a long life and last up to several decades in the body. Immunity to chickenpox, measles, and some other diseases lasts a lifetime. Immunity to many diseases eventually wears off. The immune system's response to a few diseases, such as dengue, counterproductively worsens the next infection (antibody-dependent enhancement). As of 2019, researchers are still trying to find out why some vaccines produce lifelong immunity, while the effectiveness of other vaccines drops to zero in less than 30 years (for mumps) or less than six months (for H3N2 influenza).
Memory B cells
Memory B cells are plasma cells that are able to produce antibodies for a long time. Unlike the naive B cells involved in the primary immune response, the memory B cell response is slightly different. The memory B cell has already undergone clonal expansion, differentiation and affinity maturation, so it is able to divide multiple times faster and produce antibodies with much higher affinity (especially IgG). In contrast, the naive plasma cell is fully differentiated and cannot be further stimulated by antigen to divide or increase antibody production. Memory B cell activity in secondary lymphatic organs is highest during the first 2 weeks after infection. Subsequently, after 2 to 4 weeks, its response declines. After the germinal center reaction, the memory plasma cells are located in the bone marrow, which is the main site of antibody production within the immunological memory.
Memory T cells
Memory T cells can be both CD4+ and CD8+. These memory T cells do not require further antigen stimulation to proliferate; therefore, they do not need a signal via MHC. Memory T cells can be divided into two functionally distinct groups based on the expression of the CCR7 chemokine receptor. This chemokine indicates the direction of migration into secondary lymphatic organs. Those memory T cells that do not express CCR7 (these are CCR7-) have receptors to migrate to the site of inflammation in the tissue and represent an immediate effector cell population. These cells were named memory effector T cells (TEM). After repeated stimulation they produce large amounts of IFN-γ, IL-4 and IL-5. In contrast, CCR7+ memory T cells lack proinflammatory and cytotoxic functions but express receptors for lymph node migration. These cells were named central memory T cells (TCM). They effectively stimulate dendritic cells, and after repeated stimulation, they are able to differentiate into 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. Experimental techniques used to study these cells include measuring antigen-stimulated cell proliferation and cytokine release, staining with peptide-MHC multimers, or using an activation-induced marker (AIM) assay.
Innate immune memory
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