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Allergic Rhinitis
Published in R James A England, Eamon Shamil, Rajeev Mathew, Manohar Bance, Pavol Surda, Jemy Jose, Omar Hilmi, Adam J Donne, Scott-Brown's Essential Otorhinolaryngology, 2022
In the preparation phase (sensitisation), the allergen is processed by dendritic cells and presented to T-helper 2 cells (TH2). TH2 cells release interleukins (IL-4, IL-5, IL-13 and others) that promote B-cell differentiation into plasma cells producing immunoglobulin E (IgE), which binds to mast cells receptors. Memory B cells are formed from activated B cells and are specific to the antigen encountered during the sensitisation.
The Inducible Defense System: Antibody Molecules and Antigen-Antibody Reactions
Published in Julius P. Kreier, Infection, Resistance, and Immunity, 2022
Once the antigen or infection producing the antigen is eliminated, many of the newly produced B cells will persist in an inactive state, and as a result, the person will retain a large number of B cells specific for the antigen. These cells are called memory B cells. When a person becomes infected again, a secondary response takes place. A large number of the retained memory B cells will respond. As a result of the presence of memory B cells, the secondary response is characterized by the rapid production of high affinity IgG, IgA, or IgE antibodies.
B Cells and Humoral Immunity
Published in Constantin A. Bona, Francisco A. Bonilla, Textbook of Immunology, 2019
Constantin A. Bona, Francisco A. Bonilla
Mature B cells may develop into either plasma cells or memory cells. The memory B cell is a hallmark of acquired humoral immunity. Memory is generated predominantly for Tdependent antigens, although it has also been obtained with type 2 antigens. It is possible that memory cells derive from a distinct pool of B cells. That is, one subset of mature resting B cells differentiates to plasma cells following antigen stimulation, and generates the primary response. Another subset of mature B cells is pre-destined to become memory cells. When activated, these cells rapidly switch isotype production, surface IgM and IgD are replaced by IgG, A, or E, and they then become memory cells. They then may enter a prolonged dormancy awaiting a second antigen exposure. Some have speculated that the persistence of minute amounts of antigen in the body have a role in the maintenance of the memory cell population. When activated, memory cells rapidly produce large amounts of IgG (or IgA or IgE) with high affinity for antigen. Memory cells are morphologically similar to small resting lymphocytes, but they circulate more actively from blood to lymph, and they survive for much longer periods of time between mitoses (years or decades). Memory cells are thought to constitute only about 1% of the total B cell population.
Memory B cells and long-lived plasma cells in AMR
Published in Renal Failure, 2022
Wenlong Yue, Jia Liu, Xiaohu Li, Luman Wang, Jinfeng Li
Plasma cells are differentiated from activated B cells. As the final B cells to be produced, plasma cells can be classified into short-lived plasma cells and long-lived plasma cells from GC [60]. Long-lived plasma cells produce high-affinity, class-switched antibodies, while memory B cells have broader antigen specificity. Therefore, when antigens enter the human body, long-lived plasma cells produce neutralizing antibodies against antigens in the first phase of immune response. In the second phase of immune response, memory B cells play important roles by rapidly producing antibodies with high affinity against various pathogens [50,55]. In terms of surface marker expression, CD38 and CD138 generally colocalize on the plasma cell surface [61]. Garimalla et al. [62] reported ASCs, including plasma cells and long-lived plasma cells, in peripheral blood 7 days after tetanus vaccination. These ASCs lacked CD20 expression. CD20 is specifically expressed in the late stage of B-cell development, and the failure to detect CD20 may be an indication of successful B- cell conversion into plasma cells [63,64]. After clinical transplantation, mature GC B cells and memory B cells can be eliminated from patients with AMR with drugs targeting CD20 (such as rituximab), but this treatment cannot effectively reduce the concentration of DSAs, which is consistent with the absence of CD20 molecules on the surface of plasma cells.
Success of nano-vaccines against COVID-19: a transformation in nanomedicine
Published in Expert Review of Vaccines, 2022
Manoj Kumar Sarangi, Sasmita Padhi, Gautam Rath, Sitansu Sekhar Nanda, Dong Kee Yi
Inside the lymph node, the antigens induce the adaptive immune response. They activate antigen-specific T and B cells; the latter undergoes further activation (with the support of CD4+ T cells), followed by proliferation of clones with immunoglobulin genes mutations that result in elevated antigen affinity [7,8]. High-affinity B cells differentiate into memory B cells or antibody (Ab)-producing plasma cells. Abs clear virus-infected cells (through Fc-mediated engagement), induce natural killer cells, and neutralize free virus [5,9]. Virus-infected cells are also killed by CD8+ T cells, which develop rapidly after SARS-CoV-2 infection [10]. Vaccines stimulate an increased antibody titer over time, and enduring protection against the virus relies on steady numbers of memory T and B cells.
An update on host immunity correlates and prospects of re-infection in COVID-19
Published in International Reviews of Immunology, 2022
Neema Negi, Shesh Prakash Maurya, Ravinder Singh, Bimal Kumar Das
Like the T cell compartment, the humoral component has also been shown to be significantly affected by the SARS-CoV-2 infection [142, 143] and is characterized by a marked expansion of the plasmablasts and depletion of IgM memory B cells [144] in extremely severe cases. Studies have confirmed that detectable levels of IgM, IgG and IgA could be found in the blood circulation up to 8 months after the first exposure, and neutralizing antibodies though decline over time but remain detectable post 6 months of infection [9, 145]. Interestingly, Gaebler et al. showed dynamic evolution of the memory B cell response during the first six months post SARS-CoV-2 infection. Persistence of antigen in the tissues resulted in antibody evolution via somatic mutations with increased neutralization potency. This evolution of the memory B cells would lead to a highly robust and effective immune response upon reinfection [146]. Breton et al. highlighted maintenance of polyfunctional SARS-CoV-2 specific memory immune cells and antibodies following natural infection [147, 148]. The stable maintenance memory B cell pool could provide an alternative way to help mitigate subsequent infections, although the kinetics of reinfection and protective potential of memory B cells in SARS-CoV-2 immunity are yet to be determined.