Lymphocyte population kinetics during the development of the immune system. B cell persistence and life-span can be determined by the host environment

1989 ◽  
Vol 1 (3) ◽  
pp. 237-246 ◽  
Author(s):  
Véronique Thomas-Vaslin ◽  
Antonio A. Freitas
2007 ◽  
Vol 168 (6) ◽  
pp. 725-732 ◽  
Author(s):  
L. Lacoste-Collin ◽  
S. Jozan ◽  
V. Cances-Lauwers ◽  
B. Pipy ◽  
G. Gasset ◽  
...  

2021 ◽  
Vol 10 (9) ◽  
Author(s):  
Leire de Campos‐Mata ◽  
Sonia Tejedor Vaquero ◽  
Roser Tachó‐Piñot ◽  
Janet Piñero ◽  
Emilie K Grasset ◽  
...  

2012 ◽  
Vol 188 (12) ◽  
pp. 6093-6108 ◽  
Author(s):  
Hyunjoo Lee ◽  
Shabirul Haque ◽  
Jennifer Nieto ◽  
Joshua Trott ◽  
John K. Inman ◽  
...  

2021 ◽  
Vol 118 (16) ◽  
pp. e2021570118
Author(s):  
Thiago Alves da Costa ◽  
Jacob N. Peterson ◽  
Julie Lang ◽  
Jeremy Shulman ◽  
Xiayuan Liang ◽  
...  

Central B cell tolerance, the process restricting the development of many newly generated autoreactive B cells, has been intensely investigated in mouse cells while studies in humans have been hampered by the inability to phenotypically distinguish autoreactive and nonautoreactive immature B cell clones and the difficulty in accessing fresh human bone marrow samples. Using a human immune system mouse model in which all human Igκ+ B cells undergo central tolerance, we discovered that human autoreactive immature B cells exhibit a distinctive phenotype that includes lower activation of ERK and differential expression of CD69, CD81, CXCR4, and other glycoproteins. Human B cells exhibiting these characteristics were observed in fresh human bone marrow tissue biopsy specimens, although differences in marker expression were smaller than in the humanized mouse model. Furthermore, the expression of these markers was slightly altered in autoreactive B cells of humanized mice engrafted with some human immune systems genetically predisposed to autoimmunity. Finally, by treating mice and human immune system mice with a pharmacologic antagonist, we show that signaling by CXCR4 is necessary to prevent both human and mouse autoreactive B cell clones from egressing the bone marrow, indicating that CXCR4 functionally contributes to central B cell tolerance.


2021 ◽  
Vol 12 ◽  
Author(s):  
Emily E. Radke ◽  
Zhi Li ◽  
David N. Hernandez ◽  
Hanane El Bannoudi ◽  
Sergei L. Kosakovsky Pond ◽  
...  

Staphylococcus aureus, a common cause of serious and often fatal infections, is well-armed with secreted factors that disarm host immune defenses. Highly expressed in vivo during infection, Staphylococcal protein A (SpA) is reported to also contribute to nasal colonization that can be a prelude to invasive infection. Co-evolution with the host immune system has provided SpA with an Fc-antibody binding site, and a Fab-binding site responsible for non-immune superantigen interactions via germline-encoded surfaces expressed on many human BCRs. We wondered whether the recurrent exposures to S. aureus commonly experienced by adults, result in the accumulation of memory B-cell responses to other determinants on SpA. We therefore isolated SpA-specific class-switched memory B cells, and characterized their encoding VH : VL antibody genes. In SpA-reactive memory B cells, we confirmed a striking bias in usage for VH genes, which retain the surface that mediates the SpA-superantigen interaction. We postulate these interactions reflect co-evolution of the host immune system and SpA, which during infection results in immune recruitment of an extraordinarily high prevalence of B cells in the repertoire that subverts the augmentation of protective defenses. Herein, we provide the first evidence that human memory responses are supplemented by B-cell clones, and circulating-antibodies, that bind to SpA determinants independent of the non-immune Fc- and Fab-binding sites. In parallel, we demonstrate that healthy individuals, and patients recovering from S. aureus infection, both have circulating antibodies with these conventional binding specificities. These findings rationalize the potential utility of incorporating specially engineered SpA proteins into a protective vaccine.


2010 ◽  
Vol 13 (4) ◽  
pp. 415-428 ◽  
Author(s):  
Lorena Arranz ◽  
Nuria M. De Castro ◽  
Isabel Baeza ◽  
Ianire Maté ◽  
Maria Paz Viveros ◽  
...  

1988 ◽  
Vol 167 (3) ◽  
pp. 805-816 ◽  
Author(s):  
D Gray

Currently available estimates of B cell life span vary from 4 d to 6 wk. The discrepancy may have arisen out of the selective effects of stress and drug cytotoxicity on short-lived populations. In this report, bromodeoxyuridine (BUdR), a drug that incorporates into the DNA of dividing cells, has been fed to rats in their drinking water, eliminating stressful injection procedures. Labeled cells in the recirculating B cell pool are identified in tissue sections using an mAb to BUdR. BUdR is shown to have no cytostatic effects at the dose used. Over a 5-d period of infusion, only 20% of the peripheral recirculating pool incorporate label (approximately 4% per day); labeling over various periods indicates that the peripheral B cell pool turns over in approximately 4 wk. To distinguish between turnover due to incorporation of new B cells into the peripheral pool and division of antigen-activated B cells rats underwent two consecutive periods of labeling, first with [3H]thymidine for 5 d and then with BUdR for a further 5 d. Virgin B cells newly derived from dividing precursors in the bone marrow do not continue to proliferate in the periphery, while activated cells undergo several rounds of division during both labeling periods. The results indicate that 3-4% of the peripheral pool is replaced by new B cells each day, while 0.3-0.6% become part of activated clones every day. Assuming that the peripheral pool of the rat contains 10(9) B cells, then 3-4 X 10(7) new B cells become stably incorporated per day. This represents approximately 10% of the putative output of the bone marrow.


2013 ◽  
pp. 1154-1155
Author(s):  
Véronique Thomas-Vaslin ◽  
Adrien Six ◽  
Bertrand Bellier ◽  
David Klatzmann

Gut ◽  
2020 ◽  
Vol 69 (12) ◽  
pp. 2203-2213 ◽  
Author(s):  
Anton Lutckii ◽  
Benedikt Strunz ◽  
Anton Zhirkov ◽  
Olga Filipovich ◽  
Elena Rukoiatkina ◽  
...  

ObjectivesVertical transmission of hepatitis C virus (HCV) is rare compared with other chronic viral infections, despite that newborns have an immature, and possibly more susceptible, immune system. It further remains unclear to what extent prenatal and perinatal exposure to HCV affects immune system development in neonates.DesignTo address this, we studied B cells, innate immune cells and soluble factors in a cohort of 62 children that were either unexposed, exposed uninfected or infected with HCV. Forty of these infants were followed longitudinally from birth up until 18 months of age.ResultsAs expected, evidence for B cell maturation was observed with increased age in children, whereas few age-related changes were noticed among innate immune cells. HCV-infected children had a high frequency of HCV-specific IgG-secreting B cells. Such a response was also detected in some exposed but uninfected children but not in uninfected controls. Consistent with this, both HCV-exposed uninfected and HCV-infected infants had evidence of early B cell immune maturation with an increased proportion of IgA-positive plasma cells and upregulated CD40 expression. In contrast, actual HCV viraemia, but not mere exposure, led to alterations within myeloid immune cell populations, natural killer (NK) cells and a distinct soluble factor profile with increased levels of inflammatory cytokines and chemokines.ConclusionOur data reveal that exposure to, and infection with, HCV causes disparate effects on adaptive B cells and innate immune cell such as myeloid cells and NK cells in infants.


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