ORIGINAL_ARTICLE
The Cerebrospinal Fluid Presentations of Neuro-Bechet Disease, a Way to Know the Etiopathogenesis and Improve Armamentarium
Neuro-Behcet's disease (NBD) is a rare but potentially fatal manifestation of Behcet's disease. Common presentations of neuro-Behcet's disease are parenchymal (brainstem and hemispheric manifestations, meningoencephalitis, spinal cord lesions) and non-parenchymal (arterial occlusions, aneurysms, Dural sinus thrombosis). Cerebrospinal fluid (CSF) findings in parenchymal NBD usually show an inflammatory pattern with elevated cell count (usually high levels of polymorphonuclear leukocytes), high protein, and normal glucose levels, whereas the CSF findings in non-parenchymal NBD could be normal except for high opening pressure. Further investigation of CSF in parenchymal NBD has demonstrated elevated Natural killer T cells, high inflammatory chemokines, and cytokines such as Tumor Necrosis Factor-alpha (TNF- α), Interferon-gamma (IFN-γ), Interleukin (IL)12, IL-6, IL-17, IL-26, IL-15, Vascular endothelial growth factor (VEGF), Matrix metallopeptidase 9 (MMP-9), chemokine [C-X-C motif] ligand 8 (CXC-8) which indicate the role of both innate and adaptive immunity in this disease. Particularly, T helper type 1 (TH-1) and TH-17 pathways are implicated in the pathogenesis of this condition. Successful use of certain biologic agents such as TNF and IL-6 inhibitors in NBD further emphasizes the role of inflammatory cytokines in the immunopathogenesis of the disease. Drugs blocking the TH 17 pathway such as ustekinumab, secukinumab could also be applicable in the process. This review summarizes the detailed CSF findings in NBD, current understanding of the immunopathogenesis of NBD, and treatment of NBD with specific biologic agents based on our understanding of the disease pathogenesis.
https://iji.sums.ac.ir/article_47855_e59fb5da57c7a5df578496f5a2bcb5d0.pdf
2021-09-01
170
178
10.22034/iji.2021.47855
Behcet's Syndrome
Cerebrospinal Fluid
Neuro-Behcet's Syndrome
Pathogenesis
Pathology
Shubhasree
Banerjee
mitusree@gmail.com
1
Department of Clinical Medicine, Division of Rheumatology, University of Pennsylvania, Philadelphia, PA 19104, USA.
AUTHOR
Kamel
Hamzaoui
kamel.hamzaoui@gmail.com
2
Department of Basic Sciences, Faculty of Medicine of Tunis, and Research Laboratory 19SP02 "Chronic Pulmonary Pathologies: From Genome to Management, Abderrahman Mami Hospital, Ariana, Université de Tunis El Manar Tunis, Tunisia.
AUTHOR
Anahid
Safari
safarianahid@gmail.com
3
Stem Cells Technology Research Center, Shiraz University of Medical Sciences, Shiraz, Iran.
AUTHOR
Afshin
Borhani-Haghighi
neuro.research.ab@gmail.com
4
Clinical Neurology Research Center, Shiraz University of Medical Sciences, Shiraz, Iran.
LEAD_AUTHOR
ORIGINAL_ARTICLE
Evaluation of CD4+/CD25+/high/CD127low/- Regulatory T Cells in Rheumatoid Arthritis Patients
Background: Rheumatoid arthritis (RA) is the most common rheumatoid disease of unknown etiology, determined by the articular cartilage destruction and bone loss. The hallmark of RA is the defect in immune tolerance. Regulatory T cells (Treg) play a critical role in the protection of peripheral tolerance. Objective: To assess the percentage of CD4+/CD25+/high/CD127low/- Treg cells in peripheral blood of RA patients as compared with the healthy individuals. Methods: The number of CD4+/CD25+/high/CD127low/- Treg cells was assessed by multicolor flow cytometry. The clinical disease activity of RA patients was determined by disease activity score 28 (DAS-28). The correlations of DAS-28 and erythrocyte sedimentation rate (ESR) with Treg cells were evaluated. Results: The percentage of CD4+/CD25+/high/CD127low/- Treg cells in peripheral blood of RA patients significantly decreased as compared with the healthy individuals (P= 0.0002). The percentage of CD4+/CD25+/high/CD127low/- Treg cells negatively correlated with DAS-28 and ESR. Conclusion: This study concludes that the defect of Treg cells plays a vital role in the pathogenesis of this disease. Further studies are necessary to determine the role of Treg cells in the clinical course of rheumatoid arthritis.
https://iji.sums.ac.ir/article_47845_f274371b57926902631f190326bb399b.pdf
2021-09-01
179
187
10.22034/iji.2021.68100.1365
DAS-28
Flow cytometry
Regulatory T cells
Rheumatoid Arthritis
Samaneh
Delavari
sama.delavari@gmail.com
1
Department of Immunology, School of Medicine, Ahvaz Jundishapur University of Medical Sciences, Ahvaz, Iran.
AUTHOR
Mehri
Ghafourian
mehri.ghafourian@gmail.com
2
Department of Immunology, School of Medicine, Ahvaz Jundishapur University of Medical Sciences, Ahvaz, Iran.
AUTHOR
Elham
Rajaei
elham.rajaei@gmail.com
3
Department of Internal Medicine, School of Medicine, Ahvaz Jundishapur University of Medical Sciences, Ahvaz, Iran.
AUTHOR
Karim
Mowla
karom.mowla@gmail.com
4
Department of Internal Medicine, School of Medicine, Ahvaz Jundishapur University of Medical Sciences, Ahvaz, Iran.
AUTHOR
Ata
Ghadiri
ata.ghadiri@hotmail.fr
5
Department of Immunology, School of Medicine, Ahvaz Jundishapur University of Medical Sciences, Ahvaz, Iran.
LEAD_AUTHOR
ORIGINAL_ARTICLE
The Regulation of the IL-18 on Group 2 Innate Lymphoid Cells in Allergic Rhinitis
Background: Group 2 innate lymphoid cells (ILC2s) promote allergic inflammation by producing interleukin-4 (IL-4), IL-5, IL-9, and IL-13. IL-18 can promote T helper 2 cell (Th2) response by inducing IL-4, and IL-13 production from mast cells and basophils. However, the regulation of IL-18 on ILC2s remained unknown. Objective: To investigate the regulatory role of IL-18 in inducing the type 2 innate lymphoid cells. Methods: Twenty patients with allergic rhinitis (AR) and 20 controls were enrolled. The mRNA and protein levels of IL-18 in serum, as well as the frequencies of ILC2 in peripheral blood mononuclear cells (PBMCs) were measured by real-time polymerase chain reaction (PCR), enzyme-linked immunosorbent assay (ELISA), and flow cytometry. The ILC2s were sorted and the mRNA expression of IL-18 receptor in ILC2 was analyzed by real-time PCR. The effects of IL-18 on the proliferation and type 2 cytokine production were detected by tritiated thymidine incorporation test, real-time PCR, and ELISA, respectively. Results: The levels of IL-18 mRNA and protein were significantly higher in AR patients than in the controls (P<0.05). The frequency of ILC2 in peripheral blood was elevated in the AR patients than in the controls. After stimulation by IL-18 and house dust mite (HDM), the expression of IL-18 receptor (IL-18R) by ILC2 was significantly up-regulated. The tritiated thymidine incorporation results showed that IL-18 promoted the proliferation of ILC2 in a dose-dependent manner. IL-18 also induced the expression of IL-5 and IL-13 proteins by ILC2. Conclusion: Our results confirmed -for the first time- the effect of IL-18 in innate immunity, which was demonstrated by direct effect on the differentiation and function of ILC2.
https://iji.sums.ac.ir/article_47854_33c70ddc703898a17912e3152994490b.pdf
2021-09-01
188
194
10.22034/iji.2021.85982.1734
Allergic Rhinitis
group 2 innate lymphoid cells
IL-18
Chuling
Li
chulinglidg@163.com
1
Department of Otolaryngology, Dongguan Women and Children's hospital, Dong Guan, China.
LEAD_AUTHOR
Yaxiong
Xu
xuyaxiong@163.com
2
Department of Otolaryngology, Dongguan Women and Children's hospital, Dong Guan, China.
AUTHOR
Xianglin
Luo
luoxianglin@163.com
3
Department of Otolaryngology, Dongguan Women and Children's hospital, Dong Guan, China.
AUTHOR
Fajian
Chen
chenfajian@163.com
4
Department of Otolaryngology, Dongguan Women and Children's hospital, Dong Guan, China.
AUTHOR
ORIGINAL_ARTICLE
Expression of interleukin-35 and type 2 cytokines in children with acute allergic asthma
Background: Allergic asthma is believed to be a T helper 2 cell (Th2) preponderant response caused by airway hyper-responsiveness. Interleukin-35 (IL-35) is a newly discovered anti-inflammatory cytokine. Objective: To determine whether the expression of IL-35 is associated with type-2 inflammation in children with asthma exacerbations. Methods: Thirty children (6-12 years old) with acute allergic asthma and twenty healthy controls were enrolled. Sputum was collected from lower airways. IL-35 and type 2 cytokines expression from serum and sputum were measured at mRNA and protein level by real-time PCR and enzyme-linked immunosorbent assay (ELISA), respectively. The sampling and the test were repeated eight weeks after the asthma exacerbation. Results: At the time of exacerbation, IL-35 expression decreased significantly in induced sputum and serum than in the controls. The expression of IL-35 was negatively correlated with IL-4, IL-5 and IL-13 expression. The IL-35 from induced sputum increased significantly, whereas type-2 cytokines decreased significantly eight weeks after the exacerbation. Conclusion: Our results showed that decreased IL-35 was associated with type-2 cytokines in asthma exacerbations in children, suggesting that IL-35 may be a potential future drug target for asthma exacerbations.
https://iji.sums.ac.ir/article_47853_348b228e55648f5832542abca78ec81b.pdf
2021-09-01
195
202
10.22034/iji.2021.84622.1667
Asthma
Exacerbation
Interleukin-35
Th2 Cytokines
Zhangqiao
Cai
caizhangqiaoent@163.com
1
Affiliated Renhe Hospital of China Three Gorges University
LEAD_AUTHOR
Xuxia
He
heyuxia88@163.com
2
Affiliated Renhe Hospital of China Three Gorges University
AUTHOR
Jing
Yang
yangjing@163.com
3
Affiliated Renhe Hospital of China Three Gorges University
AUTHOR
ORIGINAL_ARTICLE
Pathogenic characteristics of Th17 cells based on IL-17 signaling pathway in regulation of sebaceous gland lipoprotein metabolism in acne rat model
Background: Acne is a common and chronic inflammatory dermatosis of sebaceous gland units of the human hair follicle. Acne is closely related to immune cytokines and cells including T helper 17cells (Th17 cells). Mis-regulated glycolipid metabolism also plays a vital role in the process. Objective: This investigation aimed to explore the role of IL-17 in signaling pathways controlling sebaceous gland lipoprotein metabolism in a rat model of acne. Methods: We generated the rat ear acne model, and investigated the pathological changes of acne skin tissue by histological analysis and the changes in the critical factors including DEFB1, GPR65, FADS1, and FADS2 by Western Blot in this model. Results: There were more Th17 cells in the rat ear acne model than in the control mice. The expression levels of DEFB1, GPR65, FADS1, FADS2 and MOGAT1 were significantly upregulated in serum and tissue from rat acne model, which could be concluded that the Th17 cells play a major role in the pathogenesis of acne based. Conclusion: Although acne is associated with immune effects and glycolipid metabolism, inhibition of IL-17 signaling pathway might be a novel way for acne therapy. Our findings also suggest a new strategy for targeted therapy of acne.
https://iji.sums.ac.ir/article_47852_0b299e1df52cbaa45a35e340fd21db5e.pdf
2021-09-01
203
209
10.22034/iji.2021.88231.1855
Acne
IL-17 Signal Pathway
Metabolism
Sebaceous Gland Lipoprotein
Th17 Cells
Yanni
He
crhfxxy@163.com
1
Department of Dermatology, Minhang Hospital Affiliated to Fudan University, Shanghai, 201199, China.
AUTHOR
Qiaorong
Yang
2
Department of Dermatology, Zhongshan Hospital Fudan University, Shanghai, 200032, China.
AUTHOR
Tong
Zhang
3
Department of Dermatology, Minhang Hospital Affiliated to Fudan University, Shanghai, 201199, China.
AUTHOR
Yibin
Zeng
4
Department of Dermatology, Minhang Hospital Affiliated to Fudan University, Shanghai, 201199, China.
AUTHOR
Lingbo
Du
5
Department of Dermatology, Minhang Hospital Affiliated to Fudan University, Shanghai, 201199, China.
AUTHOR
Wuqing
Wang
wwq0711@21cn.com
6
Department of Dermatology, Minhang Hospital Affiliated to Fudan University, Shanghai, 201199, China.
LEAD_AUTHOR
ORIGINAL_ARTICLE
The association between the decreased expression levels of FOXJ1 and the activation of NF-κB pathway in interstitial lung disease of MRL/Lpr mice
Background: Pulmonary manifestations of systemic lupus erythematosus (SLE) are appearing in 4-5% of patients involving lung in almost half of the cases during the disease course. Objective: We compared the autoimmune pulmonary inflammation in the lung tissue of mice to determine the association between decreased expression levels of Forkhead Box J1 (FOXJ1) and the activation of the NF-κB pathway in autoimmune pulmonary inflammation of MRL/Lpr mice. Methods: The female BALB/c mice (n=6) and MRL/Lpr mice (n=30) were divided into 5 groups including a control group (BALB/c), and five MRL/Lpr mice groups (8W, 12W, 16W, 24W, and 32W). The infiltration of the inflammatory cells was determined in lung tissue by performing the histological analysis. The western blotting was used to examine the expression levels of the age-related FOXJ1, and p50 and p65 proteins in the lungs of MRL/Lpr mice. The expression levels of MMP2 and MMP9 were determined via immunohistochemistry and immunofluorescence. Results: There were severe infiltrates of lung cells with high levels of tracheal damage, perivascular injury and interstitial inflammatory cell infiltration when the MRL/Lpr mice from 16w to 32w comparing to the 8w old healthy MRL/Lpr mice in the control group (p <0.05). Moreover, the reduced expression levels of FOXJ1 were associated with the activation of the NF-κB pathway in interstitial lung disease of MRL/Lpr mice via the modulation of p50 and p65. In addition, the expression levels of MMP2 and MMP9 pro-inflammation factors increased in the lungs of the MRL/Lpr mice from 16w to 32w. Conclusions: The expression level of FOXJ1 might be an indicator of the degree of lung disease in lupus-prone mice.
https://iji.sums.ac.ir/article_47849_0d8c2a160681903c48660966c6c8b2da.pdf
2021-09-01
210
219
10.22034/iji.2021.89385.1944
Forkhead-box j1
interstitial lung disease
Systemic Disease
Systemic lupus erythematous
Xueqin
Wang
wangx9455@gmail.com
1
Department of Rheumatology, the Medical School of Nantong University, Nantong, China.
LEAD_AUTHOR
Yingying
Gao
ebrahim.msph@gmail.com
2
Department of Rheumatology, the First People’s Hospital of Nantong, The Second Affiliated Hospital of Nantong University, Nantong, China.
AUTHOR
Xingyu
Ge
ebrahim1340@yahoo.com
3
Department of Rheumatology, the Medical School of Nantong University, Nantong, China.
AUTHOR
Zhifeng
Gu
ebrahim2792035@gmail.com
4
Department of Rheumatology, the Medical School of Nantong University, Nantong, China.
AUTHOR
ORIGINAL_ARTICLE
Mast Cell Numbers in Primary Eosinophilic Colitis are Significantly Higher than in Secondary Tissue Eosinophilia and Normal Controls: a Possible Link to Pathogenesis
Background: Primary Eosinophilic Colitis (PEC) is one of the rare eosinophilic gastrointestinal diseases with a poorly understood pathogenesis. Eosinophilic esophagitis (EE) is the most common and best-understood disease in this category. Activated mast cells (MCs) have a role to play in the tissue damage in EE. It is not known if PEC shares this mechanism. Objective: This cross-sectional study aimed to investigate the number of MCs in PEC and to compare them with cases of secondary colonic tissue eosinophilia (TE) and normal colon. Methods: The study included 19 PEC cases, 47 cases of secondary tissue eosinophilia and 50 normal colon tissues. Histopathological slides of all cases were reviewed to confirm the diagnosis and count the number of eosinophils. Glass slides for all cases were stained for C-kit (CD117) to highlight and count the MCs. Results: The mean number of the MCs in normal controls was 9.7 MCs per HPF (SD= 4.6). The mean number of MCs in the PEC cases was 26.5 (SD=7.1) which was significantly higher than the normal counts (p-value <0.000). The mean number of MCs in the secondary TE group was 18.0 (SD=7.1), which was significantly higher than normal controls; p-value <0.000. Comparing MC counts in PEC and secondary TE also revealed a significant difference with a p-value of < 0.000. Conclusion: MCs in PEC are significantly higher than those in secondary TE and normal controls. This suggests the role of the MCs in the pathogenesis of Primary Eosinophilic Colitis.
https://iji.sums.ac.ir/article_47848_64b72d3ae4f9729adf0a18ef5045ad3c.pdf
2021-09-01
220
229
10.22034/iji.2021.88577.1881
Eosinophilia
Eosinophilic Colitis
Gastrointestinal Diseases
Mast cells
Heyam
Awad
heyamawad2000@yahoo.com
1
University of Jordan
LEAD_AUTHOR
Ammar
Sfaira
ammar_ramadan1@yahoo.com
2
School of medicine, University of Jordan
AUTHOR
Yousef
Abu Osba
abuosba1996@gmail.com
3
School of medicine, University of Jordan
AUTHOR
Mohammad
Shahin
mohammed_1996_05@hotmail.com
4
Unversity of Jordan
AUTHOR
Yousef
Al- Asa&#;d
youseftaher138@gmail.com
5
University of Jordan
AUTHOR
Nooredeen
Isbeih
noor.isbeih@hotmail.com
6
University of Jordan
AUTHOR
Maha
Shomaf
mshomaf@ju.edu.jo
7
University of Jordan
AUTHOR
Wasan
Hayagneh
wasan991@yahoo.com
8
University of Jordan
AUTHOR
ORIGINAL_ARTICLE
Overall status of Epstein-Barr virus infection, IFN-α, and TLR-7/9 in patients with Systemic Lupus Erythematosus
Background: Systemic lupus erythematous (SLE) is a multisystem autoimmune disorder. While studying the pathogenesis of SLE is prevalent, both infectious and non-infectious elements are regarded to exert an important impact on the disease's development. Objective: To explore the overall status of EBV, TLR7, TLR9, and IFN-α gene expression in 32 patients suffering from SLE and 32 healthy controls. Methods: Plasma and PBMCs were separated from fresh whole blood. To measure EBV DNA load and mRNA levels of IFN-a, TLR-7 and9 in PBMCs, molecular techniques were employed. The production of IFN-α, ds-DNA IgG antibody, and EBNA-1 IgG levels were also measured in plasma by ELISA. Results: SLE patients showed significantly higher EBV load (p=0.001) and transcriptional levels of TLR7 (p=0.0001), IFN-α (p=0.0001), and TLR9 (p=0.0001) than controls. Moreover, the plasma levels of IFN-α (p=0.0002) and EBNA-1specific IgG antibodies (p=0.01) were significantly higher in SLE patients. Conclusion: The results stressed on the potential role of EBV infection and TLRs in SLE patients although more research is needed to determine the global impact that EBV infection can have on immune signature in patients with SLE.
https://iji.sums.ac.ir/article_47847_b3c6a432e35bc64f9b7c3c0e7fc2a7eb.pdf
2021-09-01
230
240
10.22034/iji.2021.87648.1814
Epstein-Barr virus
IFN-α
Systemic lupus erythematous
Toll-Like Receptors
Sayed Mahdi
Marashi
m-marashi@tums.ac.ir
1
Virology Department, School of Public Health, Tehran University of Medical Sciences, Tehran 14155, Iran
LEAD_AUTHOR
Shima
Izadi
shimaizadi70@yahoo.com
2
Department of Virology, School of Public Health, Tehran University of Medical Sciences, Tehran, Iran.
AUTHOR
Seyed Reza
Najafizadeh
najafisr@tums.ac.ir
3
Rheumatology Research Center, Imam Khomeini hospital, Tehran University of Medical Sciences, Tehran, Iran
AUTHOR
Ahmad
Nejati
nejati_ahmad@yahoo.com
4
Department of Virology, School of Public Health, Tehran University of Medical Sciences, Tehran, Iran.
AUTHOR
Majid
Teymoori-Rad
radmajid1365@gmail.com
5
Department of Virology, School of Public Health, Tehran University of Medical Sciences, Tehran, Iran
AUTHOR
Shohreh
Shahmahmoodi
shahmahmoodi@sina.tums.ac.ir
6
Virology Division, School of Public Health, Tehran University of Medical Sciences, Tehran, Iran.
AUTHOR
Forough
Golsaz-Shirazi
forough_golsaz@yahoo.com
7
Department of Immunology, School of Public Health, Tehran University of Medical Sciences, Tehran, Iran
AUTHOR
Fazel
Shokri
fazshok@yahoo.com
8
Department of Immunology, schoolof public health,Tehran university of medical sciences, Tehran, Iran
AUTHOR
ORIGINAL_ARTICLE
Interleukin-10 Promoter and the CCR5 Polymorphisms in Iranian Azari Population with Multiple Sclerosis
Background: Changes in the expression of cytokines as the result of the single nucleotide polymorphisms (SNPs), can affect the incidence of multiple sclerosis (MS). Objective: To investigate the relationship between the frequencies of interleukin-10 (IL-10)-1082 A/G (rs1800896) and CCR5-delta32 genotypes and susceptibility to MS in the Iranian Azari population. Methods: IL-10-1082 A/G SNP and the CCR5-delta32 were genotyped in 152 patients suffering from MS and 242 healthy non-relatives by allele specific-PCR and simple PCR methods, respectively. Results: The frequencies of AA (37.6%) and AG (55.9%) genotypes of IL-10-1082 were significantly high in the control (p = 0.021) and MS patients (p = 0.015), respectively, with no statistical difference between these groups. There was no significant difference in the CCR5 gene based on the possession of wild/wild and wild/del32 genotypes between MS patients and the control group. The del32/del32 genotype was not seen in any of the investigated groups. Tobacco (cigarettes and hookahs) consumption was higher among the MS patients (p=0.004), and this has the potential to raise the risk of MS in both the individuals and their family. However, it had no significant relation with the frequency of different genotypes of the IL-10-1082 and the CCR5. Conclusion: Our finding conclude on possible role of AA genotype of IL-10 -1082 as a protective factor in MS.
https://iji.sums.ac.ir/article_47846_3a297072062ec8ac94a7c3c77304cfc4.pdf
2021-09-01
241
248
10.22034/iji.2021.83883.1634
CCR5
Delta 32
Interleukin-10
Multiple Sclerosis
Polymorphism
Mohammad
Asgharzadeh
asgharzadehmo@yahoo.com
1
Biotechnology Research Center and Faculty of Paramedicine, Tabriz University of Medical Sciences, Tabriz, Iran.
AUTHOR
Davoud
Sanajou
davoodsanajoo@gmail.com
2
Department of Clinical Biochemistry, School of Medicine, Tabriz University of Medical Sciences, Tabriz, Iran
AUTHOR
Hossein
Samadi Kafil
h.s.kafil@gmail.com
3
Drug Applied Research Center, Tabriz University of Medical Sciences, Tabriz, Iran.
AUTHOR
Mehdi
Farhoudi
farhoudi_m@yahoo.com
4
Neurosciences Research Center, Tabriz University of Medical Sciences, Tabriz, Iran
AUTHOR
Daryoush
Savadi Oskouei
savadi_d@yahoo.com
5
Neurosciences Research Center, Tabriz University of Medical Sciences, Tabriz, Iran.
AUTHOR
Fatemeh
Khaki-Khatibi
fatemehkhakikhatibi@yahoo.com
6
Department of Clinical Biochemistry, School of Medicine, Tabriz University of Medical Sciences, Tabriz, Iran
AUTHOR
Fatemeh
Ahmadi
fatemehahmadi919@gmail.com
7
Department of Biotechnology, Faculty of Advanced Medical Sciences, Tabriz University of Medical Sciences, Tabriz, Iran
AUTHOR
Manouchehr
Fadaee
m.fadaee74@yahoo.com
8
Department of Immunology, Shiraz University of Medical Sciences, Shiraz, Iran
AUTHOR
Ali
Vegari
a.vegari87@yahoo.com
9
Department of Medical Physics, Faculty of Medicine, Urmia University of Medical Sciences, Urmia, Iran.
AUTHOR
Vahid
Asgharzadeh
vahidasgharzadeh1378@gmail.com
10
Hematology and Oncology Research Center, Tabriz University of Medical Sciences, Tabriz, Iran
AUTHOR
Jalil
Rashedi
rashedijalil@gmail.com
11
Tabriz University of Medical Sciences
LEAD_AUTHOR
Behroz
Mahdavi Poor
behroz.mahdadi@gmail.com
12
Department of Laboratory Sciences, School of Paramedicine, Tabriz University of Medical Sciences, Tabriz, Iran
AUTHOR
Pourya
Gholizadeh
gholizadehp@gmail.com
13
Tabriz University of medical sciences
AUTHOR
ORIGINAL_ARTICLE
Association of three functional polymorphisms in the NLRP3 gene with susceptibility to rheumatoid arthritis in Iranian population
Background: Rheumatoid arthritis (RA) is a complex systemic autoimmune disorder with multifactorial nature. Numerous previous studies have shown that several genes are involved in the pathogenesis and increased risk of RA. The Nod-like receptor pyrin domain containing 3 (NLRP3) is involved in the regulation of innate immunity and its upregulation has previously been reported in RA. Objective: To evaluate the correlation between 3 functional polymorphisms of NLRP3 and its gene expression and RA risk. Method: One hundred and fourteen patients with RA and 120 healthy participants were recruited to this case-control study. Genotyping of rs4612666 (intronic variant), rs10754558 (3UTR variant), and rs6672995 (downstream variant) were performed applying the real‑time polymerase chain reaction high‑resolution melting (HRM) method. Results: Based on logistic regression analysis, subjects with CC genotype and C allele in rs4612666 had increased risk of RA (OR for CC genotype= 3.10; 95%CI [1.78-8.26]/ OR for C allele= 2.00; 95%CI [1.45-3.10]). Furthermore, in the patient groups, there was a significant relationship between the concentration of C-reactive protein (CRP) and rs4612666 and rs10754558 polymorphism (p < 0.05). Besides, our results revealed no significant association between the genotype and allele frequency of rs10754558 and rs6672995 and the risk of RA (P> 0.05). Conclusion: Our findings propose a significant association between rs4612666 polymorphism and increased risk of RA in the Iranian population. Moreover, rs4612666 and rs10754558 were correlated with disease activity.
https://iji.sums.ac.ir/article_47850_98bfca67eaadb1f5b34bdeaa5de8827d.pdf
2021-09-01
249
258
10.22034/iji.2021.89507.1950
Arthritis
Genotypes
Inflammasome
NLRP3 gene
Rheumatoid
Single Nucleotide Polymorphism
Mehrdad
Nasrollahzadeh Sabet
m.nasrollahzadehs@yahoo.com
1
School of Medicine, Aja University of Medical Science, Tehran, Iran.
AUTHOR
Navid
Nasrabadi
navidnasr1990@yahoo.com
2
Shahid Beheshti University of Medical Sciences, Tehran, Iran
AUTHOR
Zahra
Jalili
zjalili1995@yahoo.com
3
School of Medicine, Lorestan University, Khuram Abad, Iran
AUTHOR
Bahram
Pakzad
bpakzadd@yahoo.com
4
Division of Rheumatology, Department of Internal Medicine, School of Medicine, Isfahan University of Medical Science, Isfahan, Iran.
AUTHOR
Saeideh
Davar
zar.gene@yahoo.com
5
Department of Epidemiology and Biostatistics, School of Medicine, Urmia University of Medical Sciences, Urmia, Iran
AUTHOR
Naeim
Ehtesham
n_ehtesham2012@yahoo.com
6
Pediatric Inherited Diseases Research Center, Research Institute for Primordial Prevention of Non-communicable disease.
AUTHOR
Sima
Jafarpour
z1996hosseini@yahoo.com
7
Pediatric Inherited Diseases Research Center, Research Institute for Primordial Prevention of Non-communicable disease.
AUTHOR
Meysam
Mosallaei
me.mosallayi@uswr.ac.ir
8
Pediatric Inherited Diseases Research Center, Research Institute for Primordial Prevention of Non-communicable disease.
AUTHOR
Emran
Esmaeilzadeh
e.esmaeilzadehgene@yahoo.com
9
School of Medicine, Aja University of Medical Science, Tehran, Iran
LEAD_AUTHOR
ORIGINAL_ARTICLE
Changes of Peripheral Blood Lymphocyte Subsets and Immune Function in Children with Henoch-Schonlein Purpura Nephritis
Background: Purpuric nephritis is the most common secondary glomerular disease in childhood. Its prevalence in children has been steadily rising in recent years. Objective: To explore the characteristics and pathogenesis of changes in peripheral blood lymphocyte subsets and immune function in children with Henoch-Schonlein purpura nephritis. Methods: The study included 104 children with Henoch-Schonlein purpura, divided into nephritis (HSPN) group (68 cases) and non-nephritis (NHSPN) group (36 cases), and 15 normal children. The rate-scatter turbidimetric method was utilized to determine the immunoglobulins IgA, IgG, IgM, C3 and C4, and the flow cytometry technique was employed to detect the levels of lymphocyte subsets including CD3+, CD4+, CD8+, CD4+/CD8+, CD19+, NK, etc. Results: Compared with the control group, the CD3+, CD4+, CD8+ and NK cell levels of peripheral blood mononuclear cells significantly decreased (p <0.05), and the CD19+ level significantly elevated (p <0.05) in the HSPN group and the NHSPN group whereas the HSPN group had a more significant change than the NHSPN group (p <0.05). Compared with the control group, the serum immunoglobulin IgA and IgG of the HSPN group and the NHSPN group significantly increased, and the IgM, C3, and C4 significantly decreased (p <0.05); while the HSPN group had a more significant change than the NHSPN group (p <0.05). Conclusion: Immune dysfunction in children with HSPN is specifically manifested as low cellular immune function, which leads to increased secretion of inflammatory mediators, activates B cells, and further increases the secretion of immunoglobulins, leading to the occurrence of small vasculitis.
https://iji.sums.ac.ir/article_47856_07fe1bbdfc1ca900a37203dd6d6ed3f1.pdf
2021-09-01
259
267
10.22034/iji.2021.89742.1964
Complement
Henoch-Schonlein Purpura
Immunoglobulin
Lymphocyte Subsets
Purpuric Nephritis
QingXiao
Su
qingxiaosudrr@163.com
1
Department of Peadiatrics, The Second Hospital of HeBei Medical University, ShiJiaZhuang, China
AUTHOR
LiJun
Jiang
lijuanjiangdrr@163.com
2
Department of Peadiatrics, The Second Hospital of HeBei Medical University, ShiJiaZhuang , China
AUTHOR
Jia
Chai
jiachaidrr@163.com
3
Department of Peadiatrics, The Second Hospital of HeBei Medical University, ShiJiaZhuang , China
AUTHOR
ZhiYan
Dou
zhiyandoudrr@163.com
4
Department of Peadiatrics, The Second Hospital of HeBei Medical University, ShiJiaZhuang , China
AUTHOR
ZanHua
Rong
zanhuarongdrr@163.com
5
Department of Peadiatrics, The Second Hospital of HeBei Medical University, ShiJiaZhuang, China
AUTHOR
Xue
Zhao
xuezhaodrr@163.com
6
Department of Peadiatrics, The Second Hospital of HeBei Medical University, ShiJiaZhuang, China
AUTHOR
Bo
Yu
boyudrr@163.com
7
Department of Peadiatrics, The Second Hospital of HeBei Medical University, ShiJiaZhuang , China
AUTHOR
YuXue
Wang
yuxuewang_dr@163.com
8
Department of Peadiatrics, The Second Hospital of HeBei Medical University, ShiJiaZhuang 050000, China
AUTHOR
XinLiang
Wang
wangxinliangdrr@163.com
9
Department of Peadiatrics, The Second Hospital of HeBei Medical University, ShiJiaZhuang, China
LEAD_AUTHOR