Resting Human Memory B Cells Are Intrinsically Programmed for Enhanced Survival and Responsiveness to Diverse Stimuli Compared to Naive B Cells

Good, Kim L.; Avery, Danielle T.; Tangye, Stuart G.

doi:10.4049/jimmunol.182.2.890

Cited by 244 publications

(267 citation statements)

References 62 publications

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“…Activated B cells increased the expression levels of certain activation markers, such as CD86 and CD95 [30,31]. CD86 is a critical co-stimulatory molecule for B cell activation and CD95 is associated with apoptosis.…”

Section: Cd27mentioning

confidence: 99%

High frequencies of activated B cells and T follicular helper cells are correlated with disease activity in patients with new-onset rheumatoid arthritis

Wang

Shan

Jiang

et al. 2013

Clinical and Experimental Immunology

175

166

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Section: Cd27mentioning

confidence: 99%

High frequencies of activated B cells and T follicular helper cells are correlated with disease activity in patients with new-onset rheumatoid arthritis

Wang

Shan

Jiang

et al. 2013

Clinical and Experimental Immunology

175

166

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“…[21][22][23] In a recent study of several memory B-cell subsets in HDs, Ig class-switched CD27 ϩ B cells expressed the highest levels of activation markers and Ig class-switched CD27 Ϫ B cells expressed levels of activation markers that were intermediate between their CD27 ϩ counterpart and naive B cells. 11 Here, we observed a similar pattern for CGD patients; expression levels of activation markers CD80, CD95, and TACI were lowest on naive, intermediate on CD27 Ϫ IgG ϩ , and highest on CD27 ϩ IgG ϩ B cells (Figure 3).…”

Section: Expression Of Activation Markers On Memory B Cells Of Cgd Pamentioning

confidence: 99%

Humans with chronic granulomatous disease maintain humoral immunologic memory despite low frequencies of circulating memory B cells

Moir¹,

Ravin²,

Santich³

et al. 2012

Blood

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“…CD180 is a member of the leucine-rich repeat family of molecules with homology to Toll-like receptor 4 (14), which is highly expressed by naïve and memory B cells but not by plasma cells (15 (16), are increased in the peripheral blood of SLE patients with some correlation to disease activity (17). Considering the phenotypes of autoantibody-producing cells reported in SLE, we analyzed the expression of CD27, CD38, and CD180 on CD19 + B cells in the peripheral blood of NMO patients.…”

mentioning

confidence: 99%

Interleukin 6 signaling promotes anti-aquaporin 4 autoantibody production from plasmablasts in neuromyelitis optica

Chihara

Aranami

Sato

et al. 2011

Proc. Natl. Acad. Sci. U.S.A.

402

297

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Neuromyelitis optica (NMO) is an inflammatory disease affecting the optic nerve and spinal cord, in which autoantibodies against aquaporin 4 (AQP4) water channel protein probably play a pathogenic role. Here we show that a B-cell subpopulation, exhibiting the CD19 int CD27 high CD38 high CD180 − phenotype, is selectively increased in the peripheral blood of NMO patients and that anti-AQP4 antibodies (AQP4-Abs) are mainly produced by these cells in the blood of these patients. These B cells showed the morphological as well as the phenotypical characteristics of plasmablasts (PB) and were further expanded during NMO relapse. We also demonstrate that interleukin 6 (IL-6), shown to be increased in NMO, enhanced the survival of PB as well as their AQP4-Ab secretion, whereas the blockade of IL-6 receptor (IL-6R) signaling by anti-IL-6R antibody reduced the survival of PB in vitro. These results indicate that the IL-6-dependent B-cell subpopulation is involved in the pathogenesis of NMO, thereby providing a therapeutic strategy for targeting IL-6R signaling.neuroinflamatory disease | autoimmunity | multiple sclerosis | central nervous system | IL-6 receptor blockade N euromyelitis optica (NMO) is an inflammatory demyelinating disorder characterized by recurrent attacks of severe optic neuritis and myelitis. Unlike the conventional form of multiple sclerosis (CMS), the lesions of NMO tend to spare the cerebral white matter, especially during the early stage (1), and even a single episode of attack can cause serious neurological deficits such as total blindness and paraplegia. Accordingly, accumulation of irreversible damage to the central nervous system (CNS) along with rapid progression of disability is more frequently found in NMO compared with CMS (2).NMO can be distinguished from CMS by clinical, neuroimaging, and serological criteria (3). It is now known that serum anti-aquaporin 4 (AQP4) autoantibodies can be used as a disease marker of NMO (1, 2). AQP4 is the most abundantly expressed water channel protein in the CNS and is highly expressed in the perimicrovessel astrocyte foot processes, glia limitans, and ependyma (4). Emerging clinical and pathological observations suggest that anti-AQP4 antibodies (AQP4-Abs) play a key role in the pathogenesis of NMO. Prior studies have documented a significant correlation of serum AQP4-Ab levels with the therapeutic efficacy of plasma exchange during clinical exacerbations of NMO (2, 5). In the CNS lesions of NMO, reduced expression of AQP4 on astrocytes is evident even during the early stage (6), which is followed by the occurrence of vasculocentric destruction of astrocytes associated with perivascular deposition of complement and IgG (7).On the other hand, recent studies have suggested that AQP4-Abs alone are incapable of causing the clinical and pathological features of NMO. In fact, Hinson et al. emphasized the role of cellular immunity in combination with AQP4-Abs by showing that the attack severity of NMO was not correlated with serum AQP4-Ab levels (8). It was also d...

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Resting Human Memory B Cells Are Intrinsically Programmed for Enhanced Survival and Responsiveness to Diverse Stimuli Compared to Naive B Cells

Cited by 244 publications

References 62 publications

High frequencies of activated B cells and T follicular helper cells are correlated with disease activity in patients with new-onset rheumatoid arthritis

High frequencies of activated B cells and T follicular helper cells are correlated with disease activity in patients with new-onset rheumatoid arthritis

Humans with chronic granulomatous disease maintain humoral immunologic memory despite low frequencies of circulating memory B cells

Interleukin 6 signaling promotes anti-aquaporin 4 autoantibody production from plasmablasts in neuromyelitis optica

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