B cells from aged mice exhibit reduced apoptosis upon B-cell antigen receptor stimulation and differential ability to up-regulate survival signals

Montes, Carolina L.; Maletto, Belkys A.; Rodríguez, Eva V. Acosta; Gruppi, Adriana; Pistoresi-Palencia, María C.

doi:10.1111/j.1365-2249.2005.02969.x

Cited by 12 publications

(8 citation statements)

References 42 publications

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“…Therefore, apoptotic susceptibility of resting and activated B-lymphocytes might be differently affected IgM genes, suggesting an apparent integrity of these chronically stimulated GC B-cell compartments in aged mice (39). Finally, just recently a publication reported, in contrast to our results, no differences between young and aged mice in apoptosis percentages from freshly unactivated B-cells (40). Distinct B-cell preparations (MACS 2 selections of Bcells) as well as differences in apoptosis detection (PI staining procedures) may explain such apparent contradictory data.…”

Section: Discussioncontrasting

confidence: 56%

“…However, this study mainly focuses on BCR-mediated apoptosis which is known to occur in mature B-lymphocytes upon a strong and durable activation of cells (41). Results show a decreased apoptotic response after BCR activation of splenic B-cells in aged mice as compared to young animals, which was associated with higher levels of BCR-dependent survival signals (40). Interestingly, in the present work we also noticed that spontaneous apoptosis of activated B-cells (i.e., GC B-cells and PPs B-lymphocytes) was similar for both age groups in contrast to resting Bcells.…”

Section: Discussionmentioning

confidence: 99%

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Aged mice exhibit distinct peripheral B‐cell phenotypes differing in apoptotic susceptibility: An ex vivo analysis

Verdier¹,

Malissein²,

E³

et al. 2006

Cytometry Pt A

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Background: Age-related changes in the antibody response have been classically associated with alterations in T-cell help, but increasing evidence shows that intrinsic B-cell defects exist. This article analyzes the apoptotic susceptibility of peripheral B-cells in aged and young control mice. Materials and Methods: Freshly isolated lymphocytes from spleen and Peyer's patches (PPs) were labeled for Bcell lineage (B220 1 cells) and germinal center B subset (GCs, B2201 /PNA 1 cells). Alternatively, splenic B-cells purified by MACS were used. Apoptosis was monitored by the Annexin V binding, incorporation of 3,3 0 -dihexyloxacarbocyanine iodide (DiOC 6 (3)), propidium iodide (PI) staining, and morphological changes. Moreover, intracellular Bcl-2 expression and Bad phosphorylation status were also analyzed in B-cells. Results: We showed in aging mice an enhanced Annexin V

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Section: Discussioncontrasting

confidence: 56%

Section: Discussionmentioning

confidence: 99%

Aged mice exhibit distinct peripheral B‐cell phenotypes differing in apoptotic susceptibility: An ex vivo analysis

Verdier¹,

Malissein²,

E³

et al. 2006

Cytometry Pt A

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“…In parallel with changes in the T-cell compartment of immune tissue, there seems to be an accumulation of antigen-experienced B cells in the immunologic space that have a shrunken immunoglobulin repertoire that makes less quantity and decreased specificity of antibody to new antigen [50]. These accumulated memory B cells are CD27þ CD19þ, a marker associated with differentiation of B cells to immunoglobulin-producing cells, and as in the T-cell compartment, also may have impaired apoptosis [51][52][53]. At the same time, as a result of alteration in self-antigens due to oxidative damage and glycation, there is an increase in autoantibody production.…”

Section: Changes In B Cells In Healthy Older Adultsmentioning

confidence: 99%

Host Resistance and Immune Responses in Advanced Age

Castle

Uyemura

Fülöp

et al. 2007

Clinics in Geriatric Medicine

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Immunosenescence results in populating immune tissues with less functional T cells, and perhaps B cells dendritic cells, that do not function well and produce more type 2 cytokines and fewer type 1 cytokines. Impaired immunity, distinct from immunosenescence, correlates more with disease burden than chronologic age. Older adults who have chronic diseases or chronic infections are more susceptible to common infections and have poor vaccine responses. Understanding specific mechanisms and targeting interventions are dependent on research to resolve the relationship between frailty-associated impaired immunity and the role of chronic infection versus immunosenescence in developing impaired immunity.

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“…This was explained by a higher level of cellular FLICE-inhibitory protein (cFLIP) expression that leads to procaspase inactivation. Together, this could result in the persistence of self and nonself specific B cells (Montes et al 2006). This is correlated with the fact that B cell clonal expansion persists in old mice along with the appearance of B cell lymphomas (Szabo et al 2004).…”

Section: B Lymphocytesmentioning

confidence: 99%

Immunosupportive therapies in aging

Fülöp¹,

Larbi²,

Hirokawa³

et al. 2007

Clinical Interventions in Aging

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The primary role of the immune system is to protect the organism against pathogens, but age-associated alterations to immunity increase the susceptibility of the elderly to infectious disease. The exact nature of these changes is still controversial, but the use of screening procedures, such as the SENIEUR protocol to exclude underlying illness, helped to better characterize the changes actually related to physiological aging rather than pathology. It is generally agreed that the most marked changes occur in the cellular immune response reflecting profound alterations in T cells. Much of this is due to thymic involution as well as changes in the proportions of T cell subpopulations resulting from antigen exposure, and altered T cell activation pathways. However, a body of data indicates that innate immune responses, including the critical bridge between innate and adaptive immunity, and antigen presenting capacity are not completely resistant to senescence processes. The consequences of all these alterations are an increased incidence of infections, as well as possibly cancers, autoimmune disorders, and chronic inflammatory diseases. The leading question is what, if anything, can we do to prevent these deleterious changes without dangerously dysregulating the precarious balance of productive immunity versus immunopathology? There are many potential new therapeutic means now available to modulate immunosenescence and many others are expected to be available shortly. One main problem in applying these experimental therapies is ethical: there is a common feeling that as ageing is not a disease; the elderly are not sick and therefore do not require adventurous therapies with unpredictable side-effects in mostly frail individuals. Animal models are not helpful in this context. In this chapter we will first briefly review what we think we know about human immunosenescence and its consequences for the health status of elderly individuals. We will then discuss possible interventions that might one day become applicable in an appropriate ethical environment.

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B cells from aged mice exhibit reduced apoptosis upon B-cell antigen receptor stimulation and differential ability to up-regulate survival signals

Abstract: SummaryDuring ageing, autoimmune disorders and the higher susceptibility to infectious have been associated with alterations in the humoral immune response. We report that splenic B lymphocytes from aged mice exhibit lower level of apoptosis induced by B-cell antigen receptor (

Cited by 12 publications

References 42 publications

Aged mice exhibit distinct peripheral B‐cell phenotypes differing in apoptotic susceptibility: An ex vivo analysis

Aged mice exhibit distinct peripheral B‐cell phenotypes differing in apoptotic susceptibility: An ex vivo analysis

Host Resistance and Immune Responses in Advanced Age

Immunosupportive therapies in aging

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