2008
DOI: 10.1016/j.imbio.2007.10.005
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Activation of NF-κB in lymphocytes and increase in serum immunoglobulin in hyperthyroidism: Possible role of oxidative stress

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Cited by 28 publications
(21 citation statements)
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“…30 The results of the present study regarding hypergammablobulinemia in hyperythyroid group are consistent with results reported recently by Nandakumar et al 31 The hypergammablobulinemia in hyperythyroid patients has been associated with the activation of NF-kB in B lymphocytes through oxidative stress induced by thyroid hormones. 31 It has been also reported that higher levels of sCD23 in patients with hyperthyroidism can be attributed to generalized B-cell activation. 32 In the present study, higher serum IgE levels were observed in hypo-and hyperthyroid subjects.…”
Section: Discussionsupporting
confidence: 93%
“…30 The results of the present study regarding hypergammablobulinemia in hyperythyroid group are consistent with results reported recently by Nandakumar et al 31 The hypergammablobulinemia in hyperythyroid patients has been associated with the activation of NF-kB in B lymphocytes through oxidative stress induced by thyroid hormones. 31 It has been also reported that higher levels of sCD23 in patients with hyperthyroidism can be attributed to generalized B-cell activation. 32 In the present study, higher serum IgE levels were observed in hypo-and hyperthyroid subjects.…”
Section: Discussionsupporting
confidence: 93%
“…In agreement with these views, IR-induced (1) drastic enhancement in liver oxidative 1) drastic enhancement in liver oxidative ) drastic enhancement in liver oxidative stress status and TNF-α response; (�) loss of DNA bind-; (�) loss of DNA bind-(�) loss of DNA bind-�) loss of DNA bind-) loss of DNA binding capacity of NF-κB and STAT3, implying loss of cytoprotective potential; and (�) major increment in hepatic ; and (�) major increment in hepatic and (�) major increment in hepatic �) major increment in hepatic ) major increment in hepatic AP-1 activation, which constitutes a crucial determinant of hepatotoxicity under conditions of reduced NF-κB activation and enhanced TNF-α response, are normalized by T� treatment [26] . Similar T� actions involving other physiological functions have been described, including (1) 1) ) NF-κB activation in lymphocytes from thyroxin-treated rats [45] or hyperthyroid patients [46] in association with higher oxidative stress status and potentiation of humoral immune response; and (�) JNK/STAT3 activation by T ; and (�) JNK/STAT3 activation by T and (�) JNK/STAT3 activation by T �) JNK/STAT3 activation by T ) JNK/STAT3 activation by T� in a nutritional model of non-alcoholic steatosis in rats, with complete regression of fat accumulation [47] .…”
Section: Preconditioningsupporting
confidence: 56%
“…NF-kB) activated by oxidative stress (Nandakumar et al 2008;Morgan & Liu 2011). Based upon a variety of studies, it appears that female hosts tend to have stronger anti-oxidant defense responses than their male counterparts (Borras et al 2003;Badeau et al 2005;Vina et al 2011;Mancini et al 2013).…”
Section: Discussionmentioning
confidence: 99%