Regional specialization in the mucosal immune system: what happens in the microcompartments?

Brandtzæg, Per; Bækkevold, Espen S.; Farstad, Inger Nina; Jahnsen, Frode L.; Johansen, Finn–Eirik; Nilsen, Ellen M.; Yamanaka, Takeshi

doi:10.1016/s0167-5699(98)01413-3

Cited by 310 publications

(252 citation statements)

References 75 publications

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“…LP is considered the main effecter site where the final differentiation of IgA + B cells to IgA-secreting PCs takes place [24]. BMderived B-2 as well as PEC-derived B-1 cells have been suggested to be the origin of these IgA-producing plasma B cells [6].…”

Section: Iga-expressing B Cells Are Reduced In the Lp Of L2 Micementioning

confidence: 99%

B‐1‐cell subpopulations contribute differently to gut immunity

et al. 2013

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IntroductionIgA is the major class of Ab present in mucosal tissues of mammals. IgA constitutes a key defense mechanism against invasion by inhaled or ingested pathogens. IgA is also found at significant concentrations in the serum of many species, where it mediates the elimination of pathogens that have breached the mucosa [1].Among the various MALTs, IgA-producing cells are present in highest numbers in GALTs constituted by Peyer's patches (PPs), isolated lymphoid follicles (ILFs), and solitary intestinal lymphoid Correspondence: Dr. Bishnudeo Roy e-mail: Bishnudeo.Roy@helmholtz-hzi.de tissue (SILT) [2,3]. B cells, present in the B-cell follicles of such organized structures, form GCs upon Ag encounter. Under the influence of various cellular and molecular factors -T cells and cytokines, for instance -these B cells are thought to switch from IgM to IgA [4].Multiple pathways of IgA induction have been reported. The T-cell-dependent pathway of IgA induction is well known and, it is clear that IgA can also be induced in T-cell-independent (TI) manner (e.g. in T-cell-deficient mice, CD40 −/− mice, CD28 −/− mice, etc.) [5][6][7]. However, the precise contribution of T-cell-dependent and TI pathways to IgA production is not known.An important contribution of B-1 cells to TI responses has been suggested [6,8,9]. Peritoneal cavity (PEC) B-1 cells have also been claimed to contribute significantly to IgA-producing plasma cell (PC) Eur. J. Immunol. 2013Immunol. . 43: 2023Immunol. -2032. Importantly, according to phenotype, origin, and function, PEC B-1 cells can be divided into B-1a and B-1b subpopulations [12,13]. Phenotypically, B-1a cells are characterized as B220 lo CD19 hi IgM hi IgD lo CD43 + Mac-1 + CD5 int . B-1b cells share all the aforementioned markers with B-1a cells except CD5. With respect to differential contribution of these two B-1-cell subtypes to IgA production, recently, we could show that most of the IgA-secreting cells in the PEC of unmanipulated mice belonged to B-1b-cell subpopulation [14]. Additionally, IgA-derived VH regions from B-1b cells also contained frequent single nucleotide exchanges indicative of somatic hypermutation (SHM) [14]. Thus, a contribution of PEC B-1b cells to IgA production and hence to gut-associated immunity is quite likely. However, in spite of evidential suggestions for the contribution of B-1 cells to the intestinal PC pool, their contribution under unmanipulated conditions remains uncertain. This is partly due to the lack of appropriate markers to distinguish PCs according to their origin. In this context, a sequence-based approach to address this question should become very useful.In the present work, to investigate the participation of PEC B-1 cells in the gut-associated IgA production we have made use of the transgenic mouse model known as the L2 mouse line [15]. Mice of this line are characterized by the expression of a transgenic λ light chain obtained from the plasmacytoma MOPC315 (λ2 315 ). PEC of these mice contains almost exclusively CD5 + B-1a cells, whi...

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Section: Iga-expressing B Cells Are Reduced In the Lp Of L2 Micementioning

confidence: 99%

B‐1‐cell subpopulations contribute differently to gut immunity

et al. 2013

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“…32 The network incorporates the gut-associated lymphoid tissue (GALT), urogenital tracts, lacrimal glands, lactating mammary glands and, in the respiratory tract, the bronchus-associated lymphoid tissue (BALT), salivary glands and nasal-associated lymphoid tissue (NALT). Mucosal immunity in association with innate non-specific defence forms the first line of defence against pathogens, allergens and antigens presented at mucosal surfaces.…”

Section: Common Mucosal Immune Systemmentioning

confidence: 99%

“…Secretory IgM (SIgM) antibodies contribute to a lesser extent in the normal adult, but play a significant role in mucosal defence in the neonate and in IgA-deficiency states. 32 IgG plasma cells are in low numbers at mucosal sites but serum-derived and locally produced IgG antibodies are important in protection of the respiratory 33,34 and female genital tracts. 35 The IgA antibodies in mucosal secretions are usually in the secretory form, consisting of dimeric IgA molecules joined by J chain and containing the epithelial-derived protein, secretory component.…”

Section: Common Mucosal Immune Systemmentioning

confidence: 99%

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Exercise effects on mucosal immunity

Gleeson¹,

Pyne²

2000

Immunol Cell Biol

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SummaryThe present review examines the effects of exercise on mucosal immunity in recreational and elite athletes and the role of mucosal immunity in respiratory illness. Habitual exercise at an intense level can cause suppression of mucosal immune parameters, while moderate exercise may have positive effects. Saliva is the most commonly used secretion for measurement of secretory antibodies in the assessment of mucosal immune status. Salivary IgA and IgM concentrations decline immediately after a bout of intense exercise, but usually recover within 24 h. Training at an intense level over many years can result in a chronic suppression of salivary immunoglobulin levels. The degree of immune suppression and the recovery rates after exercise are associated with the intensity of exercise and the duration or volume of the training. Low levels of salivary IgM and IgA, particularly the IgA1 subclass, are associated with an increased risk of respiratory illness in athletes. Monitoring mucosal immune parameters during critical periods of training provides an assessment of the upper respiratory tract illness risk status of an individual athlete. The mechanisms underlying the mucosal immune suppression are unknown.

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“…This is particularly true for the gastrointestinal tract, where the large numbers of Ig-producing immunocytes in the lamina propria (LP), which constitute ϳ80% of all Ig-producing immunocytes in the body, produce dimeric IgA (dIgA) in association with the J chain (1). After binding to the polymeric Ig receptor (pIgR), a 100-kDa glycoprotein expressed on the basolateral surface of secretory epithelial cells (2), dIgA Abs are actively transcytosed to the apical cell surface following receptor-mediated endocytosis of the entire ligand-receptor complex.…”

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confidence: 99%

Role of the Polymeric Ig Receptor in Mucosal B Cell Homeostasis

Uren

Johansen

Wijburg

et al. 2003

The Journal of Immunology

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Secretory IgA (SIgA) is the most characteristic component of the mucosal immune system and has long been considered the major protective factor that prevents pathogens from invading hosts through the mucosae. Recent studies, however, have suggested that complete immunity against a range of mucosal bacterial and viral pathogens can be achieved in the absence of IgA. Therefore, to further dissect the role of SIgA, we generated mice deficient in the polymeric Ig receptor (pIgR−/− mice). As a result of an inability to transport dimeric IgA to the secretions, pIgR−/− mice are deficient in SIgA and accumulate circulating dimeric IgA, with serum levels 100-fold greater than those observed in normal mice. Examination of lamina propria mononuclear cells showed that pIgR−/− mice had ∼3 times as many IgA-secreting cells as C57BL/6 mice. Further analysis showed that these cells displayed the differentiated IgA+ B220− phenotype and accounted for a 2-fold increase in the number of lamina propria blast cells in the pIgR−/− mice. Subsequent experiments showed that OVA-specific CD4+ T cell expansion following OVA feeding was not elevated in pIgR−/− mice. Furthermore, no differences in CD8+ T cell tolerance or induction of influenza virus-specific CD8+ T cells were detected in pIgR−/− mice compared with controls. Therefore, while SIgA is clearly involved in maintaining some parameters of mucosal homeostasis in the intestine, the mechanisms associated with its barrier function and the clinical consequences of its deficiency are yet to be identified.

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Regional specialization in the mucosal immune system: what happens in the microcompartments?

Cited by 310 publications

References 75 publications

B‐1‐cell subpopulations contribute differently to gut immunity

B‐1‐cell subpopulations contribute differently to gut immunity

Exercise effects on mucosal immunity

Role of the Polymeric Ig Receptor in Mucosal B Cell Homeostasis

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