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Background: The screening efficiency of Erythrocyte indices varies in different regions. This study aimed to analyze the application efficiency of 11 Erythrocyte indices in Jiujiang prefecture. Methods: A total of 2379 patients with suspected thalassanemia were enrolled in Jiujiang Maternal and Child Health Hospital. Thalassanemia genes were detected by reverse dot blot hybridization. In addition, receiver operating characteristic curve (ROC) was used to analyze and calculate the sensitivity, specificity, Youden's Index(YI), positive likelihood ratio(+LR) , negative likelihood ratio(-LR) and area under curve (AUC) of the Erythrocyte indices. Results: 1)Thalassanemia carriers in Jiujiang prefecture mainly involved α- thalassanemia and β-thalassanemia, with the detection rate of 11.60%%. Thereinto, --SEA/αα(50.35%%) and -α3.7/αα(39.86%%) predominated in α-Thalassanemia, while the commonest gene mutation types of β-Thalassanemia were βIVS-II-654/βN, βCD41-42/βN, and βCD17/βN, accounting for 64.29%,15.87% and 9.542%, respectively. 2) Of 11 erythrocyte indices, Green and King (G&K) exhibited the highest diagnostic efficiency, with the AUC above 90%, a high sensitivity and a good specificity, which followed by England and Fraser (E&F), Sirdah(SI), Jayabose (RDW index) and Ricerca(RI). while Bessman), Ehsani(EI), Srivastava(Sriv), Shine and Lal (S&L), MentzIer(MI) and RBC count(in million) possessed a lower application value for thalassanemia screening. Conclusion: 1)Analysis of thalassanemia genotypes can provide a theoretical basis for thalassanemia screening, prenatal diagnosis and genetic counseling. 2)Compared with other erythrocyte indices, Green and King (G&K) showed higher application value for thalassanemia screening, with the largest AUC above 90%. which is considered feasible for thalassanemia screening in Jiujiang prefecture, Jiangxi province.

The ability to image adoptively transferred T cells in the body and to eliminate them to avoid toxicity will be vital for chimeric antigen receptor (CAR) T cell therapy, particularly against solid tumors with higher risk of off-tumor toxicity. Previously, we have demonstrated the utility of somatostatin receptor 2 (SSTR2) for CAR T cell imaging, illustrating the expansion and contraction of CAR T cells in tumor as well as off-tumor expansion. Using intercellular adhesion molecule 1 (ICAM-1)-specific CAR T cells that secrete interleukin (IL)-12 as a model, herein we examined the potential of SSTR2 as a safety switch when combined with the SSTR2-specific maytansine-octreotate conjugate PEN-221. Constitutive secretion of IL-12 led to continuous expansion of CAR T cells after rapid elimination of tumors, causing systemic toxicity in mice with intact MHC expression. Treatment with PEN-221 rapidly reduced the abundance of CAR T cells, decreasing the severity of xenogeneic graft-versus-host disease (GvHD), and prolonged survival. Our study supports the development of SSTR2 as a single genetic marker for CAR T cells that is readily applicable to humans both for anatomical detection of T cell distribution and an image-guided safety switch for rapid elimination of CAR T cells.

The interaction between intestinal epithelial cells (IECs) and lymphocytes is known to regulate mucosal barrier function, immune responses, and by extension, to play an etiologic role in the development of chronic inflammation in Ulcerative colitis (UC). However, the biologic function of lymphocytes and their relationship with IECs is insufficiently understood. In this study, we report, for the first time, the establishment of 3-dimensional (3D) co-culture systems of lymphocytes and mouse primary colonic organoids.C57BL/6 mice were treated with dextran sulfate sodium to induce acute colonic inflammation. Primary colonic organoids were established from cells isolated from mouse colons. Lymphocytes isolated from spleens by Ficoll density gradient assays. Colonoids and lymphocytes were co-cultured. The effects of the tested drugs on the co-culture system were assayed by Enzyme-linked Immune Sorbent Assay (ELISA) for inflammatory molecules. Inflammatory stimulation resulted in a significant increase in inflammatory cytokines in the supernatant of the colonoid-lymphocyte organoid system. Treatment with drugs known to be effective in patients with UC demonstrated a reduction in inflammatory cytokines. These findings argue that the colonoid-lymphocyte system can be utilized to model inflammation in vitro as well as for drug discovery. To validate these findings, we tested three other drugs. We produced experimental evidence that, indeed, these three drugs also induced a decrease in inflammatory cytokines of varying degrees. We report, for the first time, the successful establishment of a 3D colonoid-lymphocyte system and we validate its ability to predict the anti-inflammatory properties of several small molecules.

Background: Non-alcoholic fatty liver disease (NAFLD) is caused by excessive hepatic lipid deposition, and is characterized by hepatocyte steatosis, the accumulation of immune cells and the increased expression of inflammatory factors. Hepatic macrophages are the main hepatic immune cells, which play a decisive role in NAFLD. The inhibition of the M1 polarization of hepatic macrophages or the depletion of hepatic macrophages can alleviate hepatic steatosis and inflammation.Methods and Results: NAFLD mouse model was established by feeding high fat diet (HFD) for 16 weeks, the expression of Lrg1 in liver tissues was detected by Real-time PCR and Western blot. Then expression of Lrg1 in steatotic hepatocytes was detected by Real-time PCR and Western blot. Finally, Western-blot analysis, Real-time PCR, HE staining and immumohistochemical staining were performed to confirm the Lrg1 inhibits the activation of hepatic macrophages to alleviate NAFLD by enhancing TGF-β1 signaling. The results of present study demonstrated that Lrg1 inhibited the polarization of M1 liver macrophages induced by steatotic hepatocyte-derived conditioned medium by enhancing TGF-β1 signaling, and Lrg1 also alleviated liver inflammation induced by a high-fat diet (HFD) via TGF-β1 signaling. In addition, the expression level of Lrg1 was significantly decreased in liver tissues from mice with HFD-induced steatosis. Conclusion: Our findings identify that HFD-induced hepatic expression of Lrg1 was significantly downregulated，Lrg1 inhibits the infiltration of hepatic macrophages to alleviates fatty liver inflammation through enhancing TGF-β1 signaling.

Background Functional reprogramming of tumor-associated macrophages (TAMs) is crucial to their potent tumor-supportive capacity. However, the molecular mechanism behind the reprogramming process remains poorly understood. This work aimed to investigate the involvement of engulfment and cell motility protein 1 (ELMO1) in TAM reprogramming in colorectal cancer (CRC).Methods The expression of ELMO1 in CRC was determined by western blots and immunohistochemistry. The biological effects of ELMO1 on TAM reprogramming were evaluated in vitro. The dependence of these effects on Rac1 was assessed using a Rac1 inhibitor (NSC23766). Cell function assays were performed to determine the role of ELMO1-reprogrammed macrophages in the context of CRC progression.Results The expression of ELMO1 in stromal but not epithelial tumor cells was positively associated with advanced clinical stage and poor disease-free survival in CRC. An increase in ELMO1 expression was specifically found in TAMs, but not in other multiple non-malignant stromal cells. Gain- and loss-of-function assays indicated ELMO1 reprogrammed macrophages to a TAM-like phenotype via Rac1 activation. In turn, ELMO1-reprogrammed macrophages were shown to not only facilitate the malignant behaviors of CRC cells but exhibited potent phagocytosis of tumor cells.Conclusion ELMO1 was shown to be a crucial player for TAM reprogramming in CRC. Our work underscores the importance of ELMO1 in determining functional reprogramming of TAMs and may provide new insights on potential therapeutic strategies against CRC.

The ‘Kyoho’ grape (Vitaceae, Plantae) has large ears, plenty of flesh, and rich nutrition, and is planted across a large area in China. There are few reports on this variety in winemaking, especially on the dynamic changes of fungi in the wine fermentation broth. In this study, we used the ‘Kyoho’ grapes as raw materials and adopted a high throughput to analyze dynamic changes in fungal species composition of the natural fermentation broth at four time points: day one (D1P), day three (D3P), day five (D5P), and day fifteen (D15P). Changes in fungal metabolic pathways and the dynamic changes of dominant yeast were also analyzed. A total of 78 families, 110 genera, and 137 species were detected, in the natural fermentation broth samples. The control check (CK) had 49 families, 60 genera, and 72 species. A total of 66 differential metabolic pathways were enriched; of those 66, 41 pathways were up-regulated compared to CK, such as pyrimidine deoxyribonucleotides biosynthesis from CTP (PWY 7210), CDP-diacylglycerol biosynthesis I (PWY 5667), and chitin degradation to ethanol (PWY 7118). Changes in fungal metabolic pathways were in line with the dynamic changes of dominant yeast species in the whole process of fermentation. Pichia kluyveri , P. membranifaciens , and Citeromyces matritensis are the dominant species in the later stages of natural fermentation. These yeast species may play vital roles in the ‘Kyoho’ wine industry in the future.

Increasing studies have revealed significant associations between TOP2A with oncogenesis and prognosis of human cancers; however, pan-cancer analysis has not been reported. Here, we explored the potential carcinogenic function, the association with clinical outcomes of TOP2A in 33 different human cancers. The results showed that TOP2A was amplified in 32 investigated cancers; TOP2A expression was significantly associated with metastasis of six different cancers, and significantly associated with the survivals of patients in ten different cancers; TOP2A encoded protein was obviously upregulated in five available cancers; phosphorylated TOP2A protein at S1106 was significantly upregulated in all six available cancers. Moreover, TOP2A expression was found to be associated with the cancer-associated immune cell infiltration, including fibroblasts, Tregs and macrophages. In addition, Kyoto encyclopedia of genes and genomes (KEGG) pathway and Gene Ontology (GO) enrichment analyses revealed a most significant association between TOP2A with Wnt signaling pathway, and DNA conformation change. This work provides a comprehensive knowledge of TOP2A in different cancers, including carcinogenic function, prognostic values for metastasis and clinical outcomes.

Background: The beneficial effects of pyruvate on lactic acidosis and energy metabolism have been studied. The ability to attenuate acidosis and improve aerobic system contribution are essential for team sports athletes to perform multiple sprints in a limited time. This study aimed to investigate the impact of pyruvate supplementation on energy metabolism and lactic acidosis during high-intensity interval exercise (HIIE) and to evaluate its role in repeated sprint exercise (RSE) performance.Methods: Fourteen national-level male soccer athletes from China Football College (age: 20 ± 2 years, body fat: 13.11 ± 3.50%) participated in a randomized, double-blind, crossover study. Each subject underwent two HIIE and RSE tests after one week of supplementation with 0.1g/kg/d of pyruvate or placebo. Venous blood gas (pH, bicarbonate (HCO3-), base excess (BE) and oxygen partial pressure (pO2)) were measured at baseline, pre-HIIE, post-HIIE, pre-RSE and post-RSE. Finger-stick capillary lactate were collected at baseline, immediately after each bout of HIIE, and 3, 5, 7 and 10 min post HIIE. The energy system contributions during HIIE and exercise performance of RSE were analyzed. Results: Blood pH (p < 0.01), HCO3- (p < 0.01) and BE (p < 0.01) were significantly lower than their baseline levels at post-HIIE, pre-RSE and post-RSE in both Group pyruvate (PYR) and Group placebo (PLA), respectively. Blood pH, HCO3- and BE were significantly improved in PYR at pre-HIIE (p < 0.01), post-HIIE (p < 0.01) and pre-RSE (p < 0.01) than in PLA. Furthermore, blood BE remained higher in PYR than in PLA until the end of RSE (p < 0.05). Blood pO2 was higher at post-HIIE (p < 0.05), pre-RSE (p < 0.01) and post-RSE (p < 0.01), compared to baseline, in two groups and further higher in PYR than in PLA at post-HIIE (p < 0.05) and post-RSE (p < 0.05). During HIIE, the contribution of the aerobic system in the fourth bout of HIIE was higher in PYR than in PLA (p < 0.05). The contribution of the anaerobic energy was higher than that of the aerobic energy in PLA (p < 0.01), but without difference in PYR (p > 0.05). In addition, compared with PLA, the relative peak power (RPP) of the first and fifth sprints, the relative average power (RAP) of the fifth sprint and the average of RPP and RAP during RSE were significantly improved in PYR (p < 0.05). However, the blood lactate (p > 0.05), PD% of each bout (p > 0.05) or average PD% of RSE (p > 0.05) showed no significant difference between the two groups. Conclusion: Pyruvate supplementation with 0.1g/kg/d for a 1-week enhances aerobic metabolism and buffers exercise-induced metabolic acidosis but not lactic acidosis during HIIE, improving RSE performance in moderate acidosis. Thus, after 1 week pyruvate supplementation, athletes are expected to balance aerobic and anaerobic energy contributions and attenuate metabolic acidosis during team sports, improving exercise performance.

Background: The effects of pyruvate on metabolic acidosis and oxidative metabolism had been studied. The ability to attenuate acidosis and improve oxidative system contribution are critical to the performance of team sport athletes during perform multiple high-intensity exercise over a limited period of time. This study aimed to investigate the impact of pyruvate supplementation on energy metabolism and metabolic acidosis during high-intensity interval exercise (HIIE), as well as to evaluate its role on repeated sprint exercise (RSE) performance.Methods: 14 well-trained male college soccer athletes (age: 20 ± 2 years, body fat: 13.11 ± 3.50 %) were studied in a randomized, double-blind, cross-over study. The participants ingested either 0.1g/kg/d of pyruvate or a placebo for 1-week. Metabolic acidosis was induced by HIIE after the supplement period, and RSE ability in the acidosis state was assessed. Venous blood pH, bicarbonate (HCO3-) and base excess (BE) were measured at baseline, pre-HIIE, post-HIIE, pre-RSE and post-RSE. Finger-stick blood lactate were collected at baseline, immediately after each bout of HIIE and 3, 5, 7, 10 min after HIIE. The energy systems contribution during HIIE were estimated. Results: Blood pH, HCO3- and BE were significantly lower than baseline after HIIE (p < 0.01) in both pyruvate group (PYR) and placebo group (PLA). Compared to PLA, the blood pH, HCO3- and BE were significantly improved in PYR at pre-HIIE (p < 0.01), post-HIIE (p < 0.01) and pre-RSE (p < 0.01). Furthermore, blood BE remained higher in PYR than PLA till end of RSE (p < 0.05). The contribution of oxidative system in the fourth bout of HIIE was higher in PYR than PLA (p < 0.05). In PLA, the ratio of total anaerobic energy contribution during HIIE was higher than that of aerobic (oxidative) (p < 0.01), but not in PYR (p > 0.05). Relative peak power (RPP) of first, fifth sprint, relative average power (RAP) of fifth sprint, the average of RPP and RAP during RSE were significantly improved in PYR compared with PLA (p < 0.05). While no significant changes in the PD% of each bout (p > 0.05) or average PD% (p > 0.05) were observed between the two groups. Conclusion: Pyruvate supplementation for 1-week enhances oxidative system energy contribution and buffers metabolic acidosis during HIIE, and improves RSE performance in acidosis.

Purpose Our previous study has clarified the carcinogenic properties of arginine-specific mono-ADP ribosyltransferase 1(ART1), which is considered to be a critical post-translational modification that changes the structure and function of proteins and is widely involved in important processes. This study provides, for the first time, a comprehensive insight of transcriptomic analysis for colorectal cancer cells interfered with ART1 silencing by Illumina RNA-Seq and related verification experiments. Methods Lentiviral infection was used to construct a CT-26 cell line that stably knocks down the ART1 gene, a whole transcriptome sequencing technique was performed to identify differentially expressed genes (DEGs). GO and KEGG classification/enrichment analysis and verification experiments were performed to determine the role of ART1 in the progression of colorectal cancer. Results a total of 5552 DEGs, GO function and KEGG pathway with highest enrichment, forms of SNP and diverse splicing patterns were able to be identified. Importantly, knockdown of ART1 affected the occurrence of the splicing of certain key genes related to tumor cell growth, also down-regulated expression of the key gene PTBP1 for alternative splicing. The overall attenuation of the endoplasmic reticulum unfolded protein response (UPR) signaling pathway caused by ART1 inhibition would unbalance UPR signaling, leading to the occurrence of apoptosis to impede tumorigenesis. Conclusion ART1, which clustered in organelles, may promote the development of colorectal cancer by participating in a variety of new mechanisms including endoplasmic reticulum stress regulation, metabolic process or alternative splicing, which may provide a good clinical drug candidate closer to targeted therapy of CRC.

Background: Sepsis-induced myocardial dysfunction (SIMD), which is one of the features of multiple organ dysfunction in sepsis with extremely high mortality, is characterized by impaired myocardial compliance. To date, there are few effective treatment options to cure sepsis. Tannic acid (TA) is reportedly protective during sepsis. However, the underlying mechanisms by which TA protects against septic heart injury remains elusive. Methods: We investigated the potential effects and underlying mechanisms of TA in alleviating lipopolysaccharide (LPS)-induced H9C2 cardiomyocyte cell apoptosis. H9C2 cells were treated with LPS (15 μg/mL), TA (10 μM) and TA+LPS. Control cells were treated with media only. Apoptosis was measured using flow cytometry, RT-PCR, and Western blotting analysis. Additionally, laser confocal immunofluorescence analysis detected the production of reactive oxygen species (ROS). Western blot and RT-PCR were employed to detect ER stress-associated functional proteins. Results: The results demonstrated that TA reduced the degree of LPS-induced H9C2 cells injury, including the inhibition of ROS production and endoplasmic reticulum (ER) stress-associated apoptosis. ER stress-associated functional proteins, including ATF6, PERK, IRE1, XBP1s, and CHOP were suppressed in response to TA treatment. Furthermore, the expression levels of ER stress-associated apoptotic proteins, including JNK, Bax, Cyt, Caspase3, Caspase12, and Caspase9 were reduced following treatment with TA. Additionally, the protective effects of TA on LPS-induced H9C2 cells were strengthened following treatment with the ROS inhibitor, N-Acetylcysteine (NAC), which demonstrated that ROS-mediated ER stress-associated apoptosis and TA decreased ROS-mediated ER stress-associated apoptosis. Conclusion: Our findings demonstrated that the protective effects of TA against LPS-induced H9C2 cells apoptosis may be associated with the amelioration of ROS-mediated ER stress. These findings may assist the development of potential novel therapeutic methods to inhibit the progression of myocardial cell injury. (TA alleviates LPS-induced H9C2 cell apoptosis.)

BackgroundIt is known that type 2 diabetes mellitus patients have higher susceptibility to colorectal cancer and poorer prognosis, but the mechanism is quite unknown. Here, we investigated effect of ADP-Ribosyltransferase 1 on growth of colorectal cancer combined diabetes in high norepinephrine status and the potential mechanism. MethodsWe evaluated size and weight of transplanted tumors with different ADP-Ribosyltransferase 1 level of CT26 cells or different norepinephrine level on diabetic mice model and observed their survival time as well. Consistently, CCK8 and flow cytometry were applied for detecting growth of CT26 cells in vitro. Western blot was performed for analyzing differentially expressed proteins of proliferatic profiles to determine ADP-Ribosyltransferase 1-modulated pathway.ResultsAccording to our data, high level of norepinephrine and ADP-Ribosyltransferase 1 both facilitated proliferation of CT26 cells in vitro and in vivo, besides, inhibition of norepinephrinee-depended-proliferation was observed in ADP-Ribosyltransferase 1 silencing CT26 cells in vitro compared with CT26 cells with ADP-Ribosyltransferase 1 expression. However, we discovered after reducing norepinephrine level of serum by surgery, size and weight of the transplanted tumors were significantly reduced compared with non-operated group and sham-operated group. Further, expression of ADP-Ribosyltransferase 1, mTOR, STAT3, p-AKT protein in tumor tissues of diabetic mice was increased rather than non-diabetes mice, while after depleting norepinephrine level by renal denervation operation, expression of proliferation-relative proteins mTOR, STAT3, p-AKT protein was decreased, but no change was discovered in ADP-Ribosyltransferase 1 expression. While under the same concentration of norepinephrine environment, ADP-Ribosyltransferase 1 boosts expression of p-AKT, mTOR, STAT3, CyclinD1 and c-myc in CT26 cells in vitro. ConclusionsThis study proposed a hypothesis that high-norepinephrine-induced proliferation of colorectal cancer required expression of ADP-Ribosyltransferase 1, and raise ADP-Ribosyltransferase 1 might be a candidate target for treatment of diabetes-associated colorectal cancer.

Background: Cadherin-5 (CDH5) is aberrantly expressed in a variety of human cancers and plays an important role in angiogenesis. But its role in renal clear cell carcinoma (ccRCC) remains to be understood. Methods: The dysregulation of CDH5 expression in ccRCC and its association with clinicopathological characteristics were analyzed using the TCGA database. A meta-analysis was performed to verify the alteration of CDH5 expression in ccRCC using the GEO database. Quantitative RT-PCR and immunohistochemical staining were applied to assess the transcriptional and protein levels of CDH5. TargetScan and Tarbase were employed to predict the miRNAs with the potential to target mRNA of CDH5.Results: The mRNA level of CDH5 in ccRCC was significantly higher than in normal tissue. CDH5 mRNA expression could therefore serve as a potential diagnostic biomarker for ccRCC (AUC=0.844). However, the reduced CDH5 transcription levels were significantly correlated with patients in the T3-4 stage, lymph node and distant metastasis, as well as with a worse clinical outcome. We further observed that CDH5, at the protein level, was almost absent in ccRCC samples. In addition, a few databases screen showed that mir-27a-3p, is a highly conserved miRNA targeting CDH5. The expression of mir-27a-3p was significantly elevated in ccRCC tissues in contrast to normal tissues. Importantly, it was positively associated with the T3-4 stage and M stage, respectively, suggesting that the expression level of mir-27a-3p could serve as a diagnostic biomarker for ccRCC (AUC=0.775).Conclusion: Our data suggest that the reduced translational levels of CDH5 in ccRCC was related to the overexpression of mir-27a-3p. The higher mir-27a-3p and lower CDH5 expression significantly correlated with advanced clinical stages for ccRCC patients.

Background Acy1 Coenzyme A Acyltransferases1 (ACAT1) is a key enzyme in the metabolism of ketone bodies, but its expression and biological function in the pathogenesis of NPC remains underexplored. Methods The mRNA and protein expression levels of ACAT1 in NPC and normal control tissues were analyzed by qPCR and immunohistochemistry staining, respectively. GEO database was applied for meta-analysis of ACAT1 mRNA expression and DNA promoter methylation. The role of ACAT1 in NPC proliferation was examined by CCK8 and colony formation assays in vitro and tumorigenicity in vivo. The wound healing and transwell assays were used for analyzing the migratory and invasive ability. cDNA microarray analysis was performed to identify the genes involved in epithelial-mesenchymal transition and dysregulated by ACAT1. These changes were further confirmed by western blot. Results We found that ACAT1 is inactivated in NPC cell lines and primary tissues. DNA microarray data showed higher methylation in the CpG island region of ACAT1 in NPC than normal tissues. The demethylating reagent 5-aza-dC significantly restored the transcription of ACAT1 in NPC cell lines, suggesting that ACAT1 was inactivated by DNA promoter hypermethylation. Ectopic overexpression of ACAT1 remarkably suppressed the proliferation and colony formation of NPC cells in vitro. As well, the tumorigenesis of NPC cells overexpressing ACAT1 was decreased in vivo. In addition, the migratory and invasive capacities of NPC cells was inhibited by ACAT1 overexpression. Importantly, the higher level of ACAT1 was accompanied by an increased expression of CDH1, EPCAM, and a decreased expression of vimentin and SPARC. This strongly indicates that ACAT1 is able to affect the epithelial-mesenchymal transition in NPC, thereby controlling cellular motility. In addition, we found that ACAT1 expression increases the intracellular level of β-HB. Moreover, exogenous β-HB remarkably inhibits the growth of NPC cells in a dose-dependent manner. Conclusions We have discovered that the ketone body metabolism enzyme ACAT1 is epigenetically downregulated in NPC and acts as a potential tumor suppressor in NPC. Our findings highlight the possibility of using the modulation of ketone body metabolism as effective adjuvant therapy for NPC.

Objective Autoimmune thyroid disease(AITD) is not only an immune-related disorder, but also inherited as a complex gene-related disease. The psoriasis susceptibility 1 candidate 1(PSORS1C1) gene is a susceptibility locusin autoimmune diseases. Many autoimmune diseases have been proved to be related with the PSORS1C1 gene. However, whether the PSORS1C1 gene plays a role in affecting the predisposition to AITD remains unknown.Methods In this study, we included 1056 Chinese Han AITD patients and 954 matched healthy controls. Multiplex polymerase chain reaction (PCR) technology was used to genotype SNPs (rs3130983, rs3778638, rs3815087, rs4959053)in PSORS1C1 gene. Results An association between rs3778683 and Graves' disease (GD) was observed with statistical significance (p=0.039). The allele and genotype of single nucleotide polymorphism (SNP) rs3130983, rs3815087 and rs4959053 showed no significant association with AITDs. In addition, no linkage disequilibrium for rs3130983, rs3815087, rs3778638 and rs4959053 in PSORS1C1 gene was found between AITD patients and controls.Conclusion These data revealed the influence of PSORS1C1 on the susceptibility to AITDs and reinforced this locus as a common autoimmunity risk factor.