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Mucosal B cells and their function
Published in Phillip D. Smith, Richard S. Blumberg, Thomas T. MacDonald, Principles of Mucosal Immunology, 2020
Jo Spencer, Edward N. Janoff, Per Brandtzaeg
The Peyer's patch component of human GALT is constitutive in humans, as in mice. In humans, constitutive GALT, where clusters of B cells express CD5, can be observed in fetal intestine from around 18 weeks of gestation. Although used to identify the B-1 B-cell lineage in mice, CD5 can be expressed by immature transitional B cells in humans and can be an activation marker on human B cells (Figure 10.3). Indeed, fetal intestinal B cells are large activated cells, although there is no evidence of germinal center formation in the healthy fetal intestine. Like GALT in the postnatal intestine, B cells in fetal GALT infiltrate between the epithelial cells in the FAE, suggesting that recognition of microbial antigens is not required for this localization. However, results in originally germ-free then colonized rodents highlight the role of the microbiota in driving the magnitude of epithelial homing.
Monocyte and lymphocyte membrane markers: Ontogeny and clinical significance
Published in Gabriel Virella, Medical Immunology, 2019
Scott Sugden, Damien Montamat-Sicotte, Karen K. Yam, Joseph Murphy, Bader Yassine Diab, Virginia Litwin
Mature B cells express phenotype CD19, sIgM, and sIgD. These transitional B cells (T1, T2/T3) further develop into circulating follicular B cells in the lymph nodes. About 80% of adult B cells are found in the lymph node follicle (follicular B cells), and this population gives rise to germinal center B cells, memory B cells, and plasma cells (terminally differentiated). A small percentage of transitional B cells will differentiate into the marginal zone (MZ) B cells, which is uniquely located in the MZ of the spleen. These cells exist in a pre-activated state, enabling them to respond rapidly.
Flow Cytometry
Published in Wojciech Gorczyca, Atlas of Differential Diagnosis in Neoplastic Hematopathology, 2014
Minute subset of benign B cells in the blood, BM, and lymph nodes may express CD5. In adults, the majority of circulating B cells (B-2 cells) are CD5− (which comprise ~10% of lymphocytes), but minute subset of B cells expresses CD5. These cells (B-1 cells) can be further subdivided into CD5+ transitional B cells (“bridge” immature B cells in the BM and mature naïve B cells in the peripheral blood) and CD5+ prenaïve B cells [82]. The population of benign CD5+ B cells is prominent in fetal and infant circulation, and their number decreases significantly with age. The population of benign circulating CD5+ B cells is more prominent in pediatric population and in patients with regenerating marrow, viral infections, or certain autoimmune disorders.
How do nuclear factor kappa B (NF-κB)1 and NF-κB2 defects lead to the incidence of clinical and immunological manifestations of inborn errors of immunity?
Published in Expert Review of Clinical Immunology, 2023
Nazanin Fathi, Hanieh Mojtahedi, Marzieh Nasiri, Hassan Abolhassani, Mahsa Yousefpour Marzbali, Marzie Esmaeili, Fereshte Salami, Furozan Biglari, Nima Rezaei
The immature B-cells in the bone marrow undergo central tolerance. Positive selection occurs with the beginning of the maturation, V (D) J recombination, then the migration of cells toward secondary lymphoid organs. In the absence of positive selection signals, B cells keep light-chain rearrangements. If the antigen present in the bone marrow binds to the B cell receptor, it edits the receptor or undergoes a negative selection via apoptosis. NF-κB helps to survive the immature B-cells during the negative selection or editing phase. NF-κB1- and NF-κB2-deficient mice have been shown to have a partial reduction in immature B cells [42]. Despite the high efficiency of central tolerance, some self-reactive B-cells escape from it and migrate to the periphery. They should undergo peripheral tolerance in primary lymphoid organs. When B cells have high avidity interaction with self-antigens, it results in deletion. Still, when the avidity of the interactions is low or very low, they will become ignorant and anergy. In anergy, B cells desensitizate to BCR signaling. In this stage, some autoreactive transitional B-cells escape from the elimination of the self-reactive B-cell population. NF-κB is crucial in the splenic development of B lymphocytes, mainly by involving Bcl2 for the survival of transitional B cells [43].
Current strategies for detecting functional convergence across B-cell receptor repertoires
Published in mAbs, 2021
Matthew I. J. Raybould, Anthony R. Rees, Charlotte M. Deane
Once a naïve B-cell’s BCR has been activated through an antigen-binding event (and subsequent T-helper cell assistance), it begins to differentiate into a plasma cell, which is able to rapidly proliferate and secrete antibodies – serum-soluble BCRs. Molecular modifications associated with this transition include displaying different B-cell surface markers and a process known as ‘class switching’ – where the Fc region of the BCR swaps from an IgM or IgD isotype to an IgG, IgA, or IgE isotype. Concurrently, the B-cell migrates to the ‘germinal centre’ of the lymph nodes and on arrival yet more sequence diversity can be introduced through the process of somatic hypermutation (deliberate nucleotide mutations made throughout the receptor V domain sequence of both chains, though predominantly in the CDRs). Positive selection acts to promote mutant BCRs with higher affinity toward the antigen (‘affinity maturation’). Before or after class switching, antigen-activated B-cells can differentiate into long-lived memory cells (often characterized by expression of cell-surface protein CD2712), which persist as a high-sensitivity, low concentration population able to be reactivated and potentially undergo further maturation upon secondary infection.13 Many transitional B-cell states exist, distinguished by their expression of unique combinations of cell markers and cytokines; these were recently reviewed in detail by Sanz et al.12
Decoding intrathecal immunoglobulins and B cells in the CNS: their synthesis, function, and regulation
Published in International Reviews of Immunology, 2020
MS was traditionally considered a T cell-mediated disease, but mounting evidence over the years has implicated B cells as major players in MS immunopathogenesis [53]. The intrathecal production of antibodies leading to oligoclonal band formation in CSF is a characteristic feature of MS [28]. During their development in the bone marrow, B cells begin as immature cells which enter the blood circulation and are converted to transitional B cells [54]. These transitional cells then differentiate into naïve B cells, which upon encountering specific antigens proliferate into short-lived plasma cells (Figure 3). In the germinal centers of secondary lymphoid organs, they go through the process of class switch recombination and somatic hypermutation to become B cells that produce high-affinity antibodies [54]. A small percentage of them develop into long-lived memory B cells or plasma cells. Memory B cells and plasma cells preferentially cross the BBB of MS patients and present antigens to astrocytes, microglia, and T cells by forming ectopic lymphoid follicles, GC-like structures or meningeal tertiary lymphoid organs (TLOs) at the sites of inflammation [51]. Studies on clonal expansion and somatic hypermutation demonstrated a strong correlation between the autoreactive peripheral B cells and the intrathecal B cells present in CSF [55]. A bidirectional movement of B cells occurs between the brain and the DCL nodes across the BBB [56]. This cross-talk suggests that B cells, along with T cells, can carry antigens to DCL nodes and act as stimulators for other resting lymphocytic populations.