Journal of Clinical and Cellular Immunology
Open Access

A Short Note on Immunological Memory

Wiesław Deptuła*^{* *}Correspondence: Wiesław Deptuła*, Department of Immunology, Faculty of Biology, University of Szczecin, Szczecin, Poland, Email:

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Description

Immunological memory cells, currently represented by T and B lymphocytes and natural killer (NK) cells, which determine a rapid and effective response against a second encounter with the same antigen. Among T lymphocytes, functions of memory cells are provided by their subsets: central memory, effector memory, tissue-resident memory, and regulatory memory and stem memory T cells. Memory T and B lymphocytes are implicated in autoimmunity and maternal-fetal tolerance, as well as in immunity against microbial infections. Furthermore, evidence of immunological memory in NK cells has been established. NK cells can respond to haptens or viruses, causing antigen-specific memory cells to grow.

T, B, and NK cells, which all play a role in immunological memory, have been phenotypically and functionally defined. These cells are involved in the reaction against foreign antigens, including infections, during the secondary immune response, and play a role in autoimmune diseases, and they're also important for immunological tolerance and vaccine therapy.

Development of immunological memory

After a first immune reaction to an antigen, immunological memory develops. After a previous initial encounter to a potentially harmful agent, each individual develops immunological memory. The secondary immune response follows the same pattern as the primary immunological response. The peptide: MHC I complex am presented to neighbouring effector T cells after the memory B cell detects the antigen. It leads these cells to be become activated and proliferate quickly. The immune response's effector cells are removed after the original immune response has faded away. Antibodies, which represent the humoral component of immunological memory and serve as a crucial defence mechanism in subsequent infections, are still present in the body. A tiny number of memory T and B cells, in addition to the antibodies generated in the body, make up the cellular component of immunological memory. They stay in a relaxed position in the blood, and when they have been exposed to the same antigen again, they are able to respond quickly and destroy the antigen. Memory cells have a lengthy lifespan in the body, lasting up to several decades. Chickenpox, measles, and other infections provide lifetime immunity. Immunity too many diseases wear out over time. In some infections, such as dengue fever, the immune system's response only makes the following infection worse.

Evolution of immune memory

Memory T and B cells are a common evolutionary idea; nevertheless, the conditions required to create this costly adaptation are unique. To begin, immunological memory must have a large initial molecular machinery cost, which will necessitate reductions in other host features. Second, organisms with a medium or long lifespan have a better probability of developing such machinery. Because the immunological memory must be effective early in life, the cost of this adaptation rises if the host has a short life span.

In addition, study models suggest that the environment influences the diversity of memory cells in a population. When comparing the impact of multiple infections on a specific disease versus disease diversity in the environment, it's clear that memory cell pools accumulate diversity based on the number of individual pathogens exposed, even if it comes at the expense of efficiency when confronted with more common pathogens. Individuals who live in isolated areas, such as islands, have a smaller number of memory cells but strong immunological responses. This suggests that the environment has a significant impact on memory cell population evolution.

Memory B cells

Memory B cells are plasma cells that can generate antibodies for an extended period of time. The memory B cell response differs slightly from the naive B cells involved in the first immune response. Within the immunological memory, the memory B cell has already experienced clonal expansion, differentiation, and affinity maturation, allowing it to divide several times faster and make antibodies with considerably higher affinity (especially IgG). The naive plasma cell, on either hand, is fully differentiated and cannot be induced to divide or produce more antibodies by antigen. During the first two weeks following infection, memory B cell activity in secondary lymphatic organs is at its peak. After 2 to 4 weeks, the response begins to wane. Memory plasma cells are found in the bone marrow after the germinal centre reaction, which is the main source of antibody synthesis within the immunological memory.

Memory T cells

CD4⁺ and CD8⁺ memory T cells occur. Since these memory T cells do not require additional antigen stimulation to grow, they do not require an MHC signal. Based on the expression of the CCR7 chemokine receptor, memory T cells can be separated into two functionally distinct types. The path of migration into secondary lymphatic organs is determined by this chemokine. CCR7- memory T cells have receptors that allow them to move to the site of inflammation in the tissue and represent an immediate effector cell population. Memory effector T cells were the name given to these cells (TEM). They produce high levels of IFN-, IL-4, and IL-5 after repeated stimulation.