We know that memory cell is a very important part of our body's immunology. Once it forms, it survives in our body for a long time such as years to decades. But normal cells go for apoptosis after a certain time. Why memory cell don't go for apoptosis or what is the reason behind this long lifespan?
There is an important thing that distinguishes immune cells from the beginning when they are synthesized, matured, and prepared: which is the thymic education and clonal deletion.
Checkpoints for programmed cell death are present in lymphocytes at multiple stages of development, homeostasis, and disease prevention. The vast majority of lymphocytes never mature into fully functional cells. Stochastic recombination of gene segments for T cell receptor and Ig and heavy chains, or gene segments for TCR and Ig and light chains, is required during lymphoid development to create a unique antigen receptor for each cell, providing antigen specificity to the adaptive immune system. Due to chance genetic recombination, two out of every three coding area junctions are misjoined, preventing accurate translation. Most lymphoid cells fail to finish an in-frame antigen receptor even though they are given several chances to do so during development thanks to the usage of both loci for each antigen receptor chain and the process of receptor editing. In the absence of in-frame antigen receptors, cells are unable to respond to pre-T cell receptor and pre-B cell receptor-generated developmental cues, stop differentiating, and die via programmed cell death.
Still, not every immune response cell dies by apoptosis. Some of these cells live on to form long-term memories. While both memory and naive T cells require external cues to survive, the signals required by memory T cells appear to be distinct from those needed by naive T cells. The memory T cells do not require persistent antigen for their survival, according to the current findings. When opposed to naive T cells, memory T cells rely less on the antigen-receptor contact for their own survival. Instead, cytokines play a crucial role in keeping memory T cells alive and well. Memory CD8 T cells, for instance, were not maintained in IL-15-deficient animals, suggesting a role for this C cytokine in the long-term survival of these cells.
Clones expressing BCR with increased affinity for the immunogen are favorably selected, while B cells expressing low affinity antibodies are eliminated by apoptosis. Inducing the death of the clonally grown cells after the antigen has been removed is another important role for apoptosis to play in maintaining immune system homeostasis.
Some immunologists believe that, after each round of antigenic stimulation, the progeny of memory B cells are more likely to become plasma cells (which die) than new memory cells (which survive). In vivo, this could translate into an increased number of effector cells in the secondary and subsequent responses, and a control on the possible overexpansion of one particular memory B cell clone. However, it also means that the host might one day no longer have memory cells of this clone to call upon when the relevant pathogen strikes. In this “decreasing potential hypothesis,” immunological memory is ultimately limited. In addition, for reasons that are not yet understood, memory cells specific for different antigens have different life spans. These variations have implications for how frequently a booster shot must be given to ensure complete vaccination against a particular pathogen.
Memory cells are incredibly powerful tools for our immune system and can be very long-lived, with studies showing memory B cells for smallpox persisting at least 60 years after vaccination and for Spanish flu at least 90 years after the 1918 pandemic.
Memory B cells have several unique features including long lifespan, high sensitivity to low doses of antigen, quick and robust proliferation, and rapid differentiation into plasma cells that produce high-affinity antibodies during the secondary response.
In this sense, Md Mominul Islam , memory cells can be understood as ‚intelligent‘ or ‚learning‘ cells, imo.
Hello Md Mominul Islam
Apoptosis is crucial for immune system homeostasis, including selection and survival of long-lived antibody-forming cells and memory cells. The interactions between proapoptotic and pro-survival proteins of the Bcl-2 family are critical for this process.
Bcl-2 family members help in controlling long-term memory cell survival. BIM is a Bcl-2 homology 3 (BH3)-only protein, a pro-apoptotic protein with three major isoforms (BIM-EL, BIM-L, and BIM-S) generated from mRNA alternative splicing. BIM works in concert with other pro-apoptotic proteins, such as BAD, BAX, and anti-apoptotic proteins, such as Bcl-2, to regulate cell death and survival essential to normal tissue homeostasis.
You may want to refer to the articles attached below for better understanding.
Article Apoptosis and homeostatic control of immune responses
Article BIM-mediated apoptosis and oncogene addiction
Article A critical role for TNF receptor-associated factor 1 and Bim...
Article Convergence of TCR and cytokine signaling leads to FOXO3a ph...
https://www.biorxiv.org/content/10.1101/148437v1.full
Article Regulation of memory B-cell survival by the BH3-only protein Puma
Best.
Memory T cells, a type of immune cell, can survive for a long time in the body because they have developed mechanisms to evade apoptosis, or programmed cell death. Apoptosis is a natural process that occurs in cells when they are no longer needed or are damaged beyond repair. However, memory T cells have evolved to resist apoptosis so that they can remain in the body and provide long-lasting immunity against pathogens.
There are several reasons why memory T cells can survive for a long time:
1. Self-renewal: Memory T cells can self-renew, meaning they can divide and produce new T cells that are identical to themselves. This allows them to maintain their population in the body over time.
2. Anti-apoptotic proteins: Memory T cells express high levels of anti-apoptotic proteins, such as Bcl-2 and Bcl-xL, which prevent them from undergoing apoptosis. These proteins inhibit the activation of caspases, a family of enzymes that play a central role in inducing apoptosis.
3. Low expression of Fas: Fas is a protein that triggers apoptosis when bound by its ligand, FasL. Memory T cells express low levels of Fas, reducing their susceptibility to Fas-mediated apoptosis.
4. High expression of CD45: CD45 is a protein that regulates the activation of T cells and prevents them from undergoing apoptosis. Memory T cells express high levels of CD45, which helps them to avoid apoptosis.
5. Telomere maintenance: Telomeres are repetitive DNA sequences that protect the ends of chromosomes from degradation. Memory T cells have longer telomeres than naïve T cells, which allows them to continue dividing without losing their ability to replicate.
6. Epigenetic modifications: Memory T cells undergo epigenetic changes that silence genes involved in apoptosis, allowing them to survive for extended periods.
7. Persistence of antigen: Memory T cells can persist in the body even if the antigen that triggered their formation is no longer present. They can do this by producing cytokines that help them survive or by migrating to sites where they can be protected from apoptosis.
8. Stem cell-like properties: Some memory T cells have stem cell-like properties, which means they can self-renew and differentiate into other T cell subsets. This allows them to maintain their populations in the body over time.
In summary, memory T cells have developed multiple strategies to evade apoptosis and ensure their survival in the body for a long time. These mechanisms allow them to provide long-lasting immunity against pathogens and protect us from reinfection.
Good Luck, All the best
Memory cells, whether they are memory B cells or memory T cells, can survive in the body for long periods of time, sometimes for decades, providing long-term immunity against pathogens. Several mechanisms contribute to the survival of memory cells. Memory cells are typically in a quiescent (non-dividing) state, which allows them to persist for extended periods without undergoing apoptosis (cell death). This quiescent state is maintained by various signals, including cytokines and survival factors.
Memory cells, a type of immune cell, are crucial for the body's ability to remember and respond more effectively to previously encountered pathogens. These cells, particularly memory T and B cells, can survive for extended periods within the body due to several mechanisms: the ability of memory cells to enter a quiescent state, undergo homeostatic proliferation, receive survival signals, strategically located within the body, and rapidly respond to antigen re-encounter contributes to their long-term survival and function in providing immune memory.
- Badges
- Science topic
- Similar topics
- Engineering
- Materials Engineering
- Powders