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Reversing B cell aging.

Mehr R, Melamed D - Aging (Albany NY) (2011)

Bottom Line: The mechanisms leading to these changes are poorly understood.Recently, we have shown that these changes reflect, at least in part, homeostatic pressures imposed by long-lived B cells that accumulate with aging, and that aging in the B lineage can be reversed upon alteration of B cell homeostasis by depletion.Here we discuss homeostatic causes for B lineage immunosenescence, and the potential for its rejuvenation.

View Article: PubMed Central - PubMed

Affiliation: The Mina and Everard Goodman Faculty of Life Sciences, Bar-Ilan University, Ramat-Gan 52900, Israel.

ABSTRACT
Age-related alterations in the cellular composition of the B lineage are a major cause of the poor antibody response to vaccination and to infectious agents among the elderly population. The mechanisms leading to these changes are poorly understood. Recently, we have shown that these changes reflect, at least in part, homeostatic pressures imposed by long-lived B cells that accumulate with aging, and that aging in the B lineage can be reversed upon alteration of B cell homeostasis by depletion. Here we discuss homeostatic causes for B lineage immunosenescence, and the potential for its rejuvenation.

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Related in: MedlinePlus

Based on our results we hypothesize that homeostatic pressures regulate the cellular composition of stem and B lineage cell compartments in aging. We suggest that these homeostatic pressures are set by the long lived B cells accumulating in the periphery with aging to alter the stem cell compartment and to suppress B lymphopoiesis. Changing the homeostatic equilibrium by depletion of B cells in old mice, increases frequencies of lymphoid-committed stem cells to reactivate B lymphopoiesis and to increase B cell output from the BM to the periphery. The nature of these cross-talk homeostasis mechanisms is yet to be defined, but our results suggest that they are sensed by the stem cell compartments.
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Figure 1: Based on our results we hypothesize that homeostatic pressures regulate the cellular composition of stem and B lineage cell compartments in aging. We suggest that these homeostatic pressures are set by the long lived B cells accumulating in the periphery with aging to alter the stem cell compartment and to suppress B lymphopoiesis. Changing the homeostatic equilibrium by depletion of B cells in old mice, increases frequencies of lymphoid-committed stem cells to reactivate B lymphopoiesis and to increase B cell output from the BM to the periphery. The nature of these cross-talk homeostasis mechanisms is yet to be defined, but our results suggest that they are sensed by the stem cell compartments.

Mentions: The major conclusion of our study is that age-related alterations in the B lineage are reversible and mediated by homeostatic pressures imposed by the long-lived B cells accumulating in the periphery with age (figure 1). These observations are the foundations of new paradigms for enhancing immune responsiveness in aging, which may be translated in the future for clinical use. The nature of these homeostatic regulation mechanisms and the cross-talk between peripheral B cells and progenitor cell populations in the BM are yet to be identified. This will allow direct manipulation of B cell homeostasis by targeting the regulatory factor(s) rather than by depletion of B cells, to reactivate B lymphopoiesis and to enhance immune competence in the elderly.


Reversing B cell aging.

Mehr R, Melamed D - Aging (Albany NY) (2011)

Based on our results we hypothesize that homeostatic pressures regulate the cellular composition of stem and B lineage cell compartments in aging. We suggest that these homeostatic pressures are set by the long lived B cells accumulating in the periphery with aging to alter the stem cell compartment and to suppress B lymphopoiesis. Changing the homeostatic equilibrium by depletion of B cells in old mice, increases frequencies of lymphoid-committed stem cells to reactivate B lymphopoiesis and to increase B cell output from the BM to the periphery. The nature of these cross-talk homeostasis mechanisms is yet to be defined, but our results suggest that they are sensed by the stem cell compartments.
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC3117459&req=5

Figure 1: Based on our results we hypothesize that homeostatic pressures regulate the cellular composition of stem and B lineage cell compartments in aging. We suggest that these homeostatic pressures are set by the long lived B cells accumulating in the periphery with aging to alter the stem cell compartment and to suppress B lymphopoiesis. Changing the homeostatic equilibrium by depletion of B cells in old mice, increases frequencies of lymphoid-committed stem cells to reactivate B lymphopoiesis and to increase B cell output from the BM to the periphery. The nature of these cross-talk homeostasis mechanisms is yet to be defined, but our results suggest that they are sensed by the stem cell compartments.
Mentions: The major conclusion of our study is that age-related alterations in the B lineage are reversible and mediated by homeostatic pressures imposed by the long-lived B cells accumulating in the periphery with age (figure 1). These observations are the foundations of new paradigms for enhancing immune responsiveness in aging, which may be translated in the future for clinical use. The nature of these homeostatic regulation mechanisms and the cross-talk between peripheral B cells and progenitor cell populations in the BM are yet to be identified. This will allow direct manipulation of B cell homeostasis by targeting the regulatory factor(s) rather than by depletion of B cells, to reactivate B lymphopoiesis and to enhance immune competence in the elderly.

Bottom Line: The mechanisms leading to these changes are poorly understood.Recently, we have shown that these changes reflect, at least in part, homeostatic pressures imposed by long-lived B cells that accumulate with aging, and that aging in the B lineage can be reversed upon alteration of B cell homeostasis by depletion.Here we discuss homeostatic causes for B lineage immunosenescence, and the potential for its rejuvenation.

View Article: PubMed Central - PubMed

Affiliation: The Mina and Everard Goodman Faculty of Life Sciences, Bar-Ilan University, Ramat-Gan 52900, Israel.

ABSTRACT
Age-related alterations in the cellular composition of the B lineage are a major cause of the poor antibody response to vaccination and to infectious agents among the elderly population. The mechanisms leading to these changes are poorly understood. Recently, we have shown that these changes reflect, at least in part, homeostatic pressures imposed by long-lived B cells that accumulate with aging, and that aging in the B lineage can be reversed upon alteration of B cell homeostasis by depletion. Here we discuss homeostatic causes for B lineage immunosenescence, and the potential for its rejuvenation.

Show MeSH
Related in: MedlinePlus