The IL family is also named the

The IL-2 family is also named the γ-chain (γc) family because the receptors for these cytokines share γc (also known as IL-2Rγ and CD132), which consists of IL-2, IL-4, IL-5, IL-7, IL-9, IL-15 and IL-21 [21]. Both circulating IL-2 and aortic IL-2 receptor are reported to increase in type A AD when compared with control subjects, and the IL-2 receptor negatively correlated with the follow-up period after repair [22, 23]. Our recent study showed that both circulating Th2/Th9 cells and their functional cytokines IL-4/IL-9 were reduced in human AD [24]. IL-5, IL-7, IL-15 and IL-21 were not reported to be involved in AD. Members of the IL-6 superfamily include IL-6, IL-11, IL-30, IL-31 and non-IL molecules, such as leukemia inhibitory factor (LIF), oncostatin M (OSM), ciliary neurotrophic factor (CNTF), cardiotrophin-1 (CT-1), cardiotrophin-2 (CT-2) and cardiotrophin-like cytokine (CLC) [25, 26]. The IL-6 family is characterized by their receptors, which share the GP130 subunit [26]. Data from clinical experiments and animal studies showed that both circulating and aortic IL-6 mRNA levels were elevated with AD [15, 17, 23, [27], [28], [29], [30]]. In addition, IL-6 could activate the signal transducer and activator of the transcription-3 pathway, promote Th17 infiltration of the gnrh antagonist and enhance Ang II-induced AD in mice [31]. In another study, the authors found that IL-6 expression was significantly increased when compared to the controls and was accompanied by up-regulated autophagy in the human TAD aortic wall; down-regulation of IL-6 expression could repress expression of the VSMC contractile proteins α-SMA and SM22α via enhancement of autophagy-related 4B cysteine peptidase (ATG4B)-mediated autophagy in vitro [32]. In our recent study, we found that IL-11 was elevated in both plasma and the aortas of AD patients and that macrophages were the source of IL-11; this IL-11 may participate in AD via promotion of IFN-γ and IL-17 secretion [33]. Studies between other IL-11 members and AD have not yet been reported. The IL-10 family consists of nine related molecules: IL-10, IL-19, IL-20, IL-22, IL-24, IL-26, IL-28α, IL-28β, and IL-29 [34]. These molecules have a somewhat conserved primary structure and contain a core of hydrophobic amino acids and two pairs of disulfide bonds in the chain, giving them a similar spatial conformation and thus enabling them to bind type II cytokine receptors [35]. Among these IL-10 family members, IL-10 and IL-22 were reported to be closely related to AD. The expression of IL-10 in AD is controversial. There was only one early article that reported that IL-10 was decreased in a pig AD model [15], while an opposing trend was observed in human AD among other studies [23, [36], [37], [38], [39], [40], [41]]. In addition, using an Ang II-induced mouse AD model, IL-10 could play an anti-inflammatory role and alleviate the progression and development of AD [42]. In our previous study, we found that plasma IL-22 levels were increased in AD patients, and higher aortic IL-22 levels were also observed in the torn section [30]. In another recently published paper, we found that both Th22 and IL-22 levels were increased in AD patients and were positively correlated with the occurrence of AD [21].