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Cited by 122 publications
(78 citation statements)
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“…Elimination of NLRP3 or ASC attenuates this age-related thymic atrophy and promotes T cell repertoire diversity [139]. In addition to the dysregulation of T cell homeostasis, age-associated B cell expansion in adipose tissues impairs tissue metabolism and promotes visceral adiposity in the elderly, a process regulated by the NLRP3 inflammasome [140]. Together, these two studies suggest that targeting the NLRP3 inflammasome has a potential beneficial effect on the re-establishment of immune competence in the elderly.…”
Section: Nlrp3 Inflammasome and Inflammagingmentioning
confidence: 99%
“…Elimination of NLRP3 or ASC attenuates this age-related thymic atrophy and promotes T cell repertoire diversity [139]. In addition to the dysregulation of T cell homeostasis, age-associated B cell expansion in adipose tissues impairs tissue metabolism and promotes visceral adiposity in the elderly, a process regulated by the NLRP3 inflammasome [140]. Together, these two studies suggest that targeting the NLRP3 inflammasome has a potential beneficial effect on the re-establishment of immune competence in the elderly.…”
Section: Nlrp3 Inflammasome and Inflammagingmentioning
confidence: 99%
“…B cells infiltrate the AT under obesity conditions ( 25 , 26 , 54 ), recruited by several chemotactic signals including those generated by the interaction of the leukotriene B4 with its receptor. Inhibition of this interaction has been shown to reduce B cell recruitment and activation and to mitigate the contribution of B cells to local inflammation and IR ( 55 ).…”
Section: Effects Of Obesity On Mouse B Cellsmentioning
confidence: 99%
“…AT-associated B cells are highly inflammatory and secrete several pro-inflammatory mediators (cytokines, chemokines, adipokines). It has recently been shown that aging further increases the expansion of these AT resident B cells, through the activation of the NLRP3 inflammasome, a major regulator of inflammaging and age-associated metabolic disorders, likely due to AT-associated metabolic and mitochondria dysfunction and increased production of mitochondrial reactive oxygen species ( 54 ). Our studies on mice fed HFD have confirmed the above findings and have shown that the increased size of the AT, increased infiltration of immune cells and increased secretion of pro-inflammatory mediators induce a powerful feed-forward loop of inflammation, both locally and systemically, that are responsible for the refractory response of immune cells to further in vivo and in vitro stimulation.…”
Section: Effects Of Obesity On Mouse B Cellsmentioning
confidence: 99%
“…Caspase-1 is critical for proteolytic activation and secretion of pro-inflammatory cytokines IL1β and IL-18 [61,62]. The presence of FFAs in adipose tissue can induce activation of inflammasome [61] and its essential role in metabolic disturbances has become clear [61,63,64]. A very recent work demonstrated that the absence of these three critical inflammasome components, Nlrp3, ASC, and caspase-1, in mice protects mice from HFD-induced obesity, insulin resistance, and adipocyte hypertrophy [64].…”
Section: Discussionmentioning
confidence: 99%