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Title: Associations between IL-12β rs3212227 polymorphism and susceptibility to psoriasis: a meta-analysis
Running title: Association of IL-12β rs3212227 and psoriasis
Abstract
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Purpose The aim of this meta-analysis was to explore whether IL-12β rs3212227 polymorphism confer susceptibility to psoriasis.
Methods We performed a computerized literature search before December 2013. Review Manger 5.2 was used to perform meta-analysis. The meta-analysis was conducted on the associations between IL-12β rs3212227 polymorphism and the risk of psoriasis.
Results Nine studies involving 17,620 subjects were included in this meta-analysis. Significant association was found between psoriasis and IL-12β rs3212227 allele in all study subjects (C vs. A: OR=0.68, 95%CI =0.64-0.72, P<0.01; CC+AC vs. AA: OR=0.61, 95%CI =0.53-0.71, P<0.01; CC vs. AC+AA: OR=0.53, 95%CI =0.43-0.66, P<0.01; CC vs. AA: OR=0.46, 95%CI =0.36-0.57, P<0.01; AC vs. AA: OR=0.65, 95%CI =0.59-0.71, P<0.01). Subgroup analysis showed that the association of IL-12β rs3212227 polymorphism with psoriasis existed in Asian and European.
Conclusions This meta-analysis demonstrated that the IL-12β rs3212227 polymorphism is associated with the risk of psoriasis.
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Keywords IL-12β, polymorphism, psoriasis, Meta-analysis, susceptibility gene
Introduction
Psoriasis is an immune-mediated chronic inflammatory skin disease, characterized by epidermal hyperplasia and infiltration of leukocytes into the dermis and epidermis [1]. An recent systematic review [2] reported that the prevalence in children ranged from 0% (Taiwan) to 2.1% (Italy), and in adults it varied from 0.91%(United States) to 8.5% (Norway). In children, the incidence estimate reported (United States) was 40.8/100,000person-years. In adults, it varied from 78.9/100,000 person-years (United States) to 230/100,000 person-years (Italy).
It reported that psoriasis occurred by the interaction between genetic and environmental factors [3] and the immune mechanism plays an essential role in the chronic development and progression of psoriasis [4]. However, until now the exact etiology and pathogenesis of psoriasis remain unclear [5]. Currently, the study of psoriasis susceptibility genes is a hot research direction.
IL-12 is a kind of key cytokines involved in T cell immune [6]. It confirmed thatIL -12 is closely related to the pathogenesis of psoriasis . rs3212227 is a SNP in 3’ untranslated region [7]. Tsunemi et al. [8] reported the association of rs3212227 with risk of psoriasis. Capon et al. reported that there was significant association between rs3212227 and psoriasis. It indicated that IL-12β rs3212227 may be one of the psoriasis susceptibility genes. The aim of this meta-analysis was to determine whether IL-12β rs3212227 polymorphisms confer susceptibility to psoriasis.
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Methods
Literature search
A literature search was conducted using PubMed, Medline and Embase up to December 2013. We screened all fields by combining the term “psoriasis” or “psoriatic”, “interleukin-12β” or “IL-12β” and “genetic polymorphism” or “genetic variant”.
Selection criteria
Literatures were included in this meta-analysis if they met each of the following criteria: (1) case-control studies between patients with psoriasis (experimental group) and hospital-based or population-based individuals (control group), (2) published English literatures involving studies of association between IL-12β genetic polymorphism and psoriasis, and (3) having the data of genotype and frequency of allele in the experimental and control group or obtaining by computing. Studies were excluded when genotype distribution in the control group did not meet the test of hardy-weinberg equilibrium.
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Data extraction and quality assessment
Data extraction was conducted by two reviewers independently. Disagreements between reviewers were resolved by discussion with a third investigator. From the included studies, the following data were abstracted: the first author name, year of publication, country or race, genotype distribution inthe experimental and control group, gender ratio and mean age of the subjects in the experimental and control group. In this meta-analysis, we applied the criteria based on Clark et al [9] to assess the quality of included studies. On the basis of their scores, the included studies were classified into three levels: low quality (0-4), moderate quality (5-7)and high quality (8-10).
Statistical analysis
Test of hardy-weinberg equilibrium [10] was conducted to ensure the quality of the included literatures before running meta-analysis. Review Manger 5.2 was used to perform meta-analysis. Odds ratios (ORs) with 95 % confidence intervals (CIs) were calculated under five genetic models: the allele model (C vs. A), the dominant model (CC+AC vs. AA), the recessive model (CC vs. AA+AC), the homozygous/additive model (CC vs. AA) and the heterozygous model (CC vs. AC). Heterogeneity was evaluated using by the chi-square-based Q statistic test [11] and I2 test with α<0.05. Fixed-effect models were used to pool the data unless statistical heterogeneity was significant, in which case a random effect model was used [12]. Subgroup analysis was performed by the difference of ethnicity. The sensitivity analysis was conducted to see the stability of pooled results by sequential omission of individual studies [13]. Funnel plots were used to assess the possibility of publication bias.
Results
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In total, 114 potentially relevant studies were identified and screened after an initial search. Among them, 98 articles were excluded after screening based on abstracts or titles. Five out of these 16 remaining literatures were excluded because of duplicate publication. Then 2 studies were removing because there was no available data. As a result, 9 literatures were included in this meta-analysis. A flow diagram of the search process is shown in Fig.1.
Characteristics of included studies
The characteristics of 9 included studies [8, 14-21] were summarized in Table 1. The publication years of these studies ranged from year 2002 to 2013. A total of 17,620 subjects were involved in this meta-analysis, including 6,520 psoriasis patients and 11,150 healthy controls. The race of these subjects was Caucasian or Asian except one study in which mix racial subjects were studied. None of the SNPs had genotype frequencies that deviated significantly from Hardy–Weinberg equilibrium in these included studies. All quality scores of included studies were from 5 to 8. It showed that the included studies were moderate–high quality literatures in this meta-analysis.
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Meta-analysis of the association between IL-12β rs3212227 polymorphism and psoriasis
Summary results of this meta-analysis for the association between IL-12β rs3212227 polymorphism and psoriasis were shown in Table 2. For the genotype model of CC+AC vs. A, no heterogeneity (I2=57%, P=0.02) existed in the included literatures, so the random effects model was used. For the other genotype model, fixed effects model was used because of significant heterogeneity among studies.
The meta-analysis results showed the highly significant association of these alleles with psoriasis (C vs. A: OR=0.68, 95%CI =0.64-0.72, P<0.01, Fig.1; CC+AC vs. AA: OR=0.61, 95%CI =0.53-0.71, P<0.01; CC vs. AC+AA: OR=0.53, 95%CI =0.43-0.66, P<0.01; CC vs. AA: OR=0.46, 95%CI =0.36-0.57, P<0.01; AC vs. AA: OR=0.65, 95%CI =0.59-0.71, P<0.01). Further subgroup analysis indicated that there were significant association between IL-12β rs3212227 polymorphism and psoriasis in European group (C vs. A: OR= 0.66, 95%CI =0.61-0.70, P<0.01; CC+AC vs. AA: OR=0.62, 95%CI =0.52-0.73, P<0.01; CC vs. AC+AA: OR=0.48, 95%CI =0.36-0.64, P<0.01; CC vs. AA: OR=0.42, 95%CI =0.31-0.56, P<0.01; AC vs. AA: OR=0.62, 95%CI =0.56-0.69, P<0.01) and Asian group (C vs. A: OR= 0.71, 95%CI =0.62-0.82, P<0.01; CC+AC vs. AA: OR=0.45, 95%CI =0.25-0.82, P<0.01; CC vs. AC+AA: OR=0.56, 95%CI =0.36-0.85, P<0.01; CC vs. AA: OR=0.43, 95%CI =0.26-0.70, P<0.01; AC vs. AA: OR=0.66, 95%CI =0.44-0.98, P<0.01) (Table 2).
Sensitivity analysis and publication bias
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Sensitivity analysis by dropping one study at a time did not indicate the dominant influence of any single study. The funnel plot showed that there was no obvious publication bias was shown in the result.
Discussion
In this meta-analysis, we combined data from published studies to evaluate genetic associations between polymorphisms of IL-12β rs3212227 and psoriasis. Our meta-analysis of IL-12β rs3212227 showed significant association of the IL-12β rs3212227 polymorphisms with the risk of psoriasis. Another meta-analysis [22] reported the association of IL-12β rs3212227 and psoriasis. Compared with that one, there were three the advantages of this meta-analysis. The first one was that this meta-analysis had been more recently (2013) conducted to synthesize evidence concerning the association of IL-12β rs3212227 and psoriasis. Second, furthermore subgroup analysis by ethnicity was performed and showed that the results did not varies with the difference of ethnicity. Third, the publication meta-analysis reported no heterogeneity among the included studies. Nevertheless, in this meta-analysis, heterogeneity was found among the included studies in the genotype model of CC+AC vs. AA. Exploring the sources of heterogeneity was useful to study the association of IL-12β rs3212227 and psoriasis. Thus, further well-designed studies need to focus on exploring the sources of heterogeneity.
In the publication studies, it demonstrated that IL-12 was closely related to the pathogenesis of psoriasis. It reported that the mRNA [23]and protein expression [24] of IL-12 p40 was increased in the psoriatic skin. Efficacy was obtained by the drug therapy on immunization targets [25]. The SNP, rs3212227, is located in IL-12β gene [26]. The expression of IL-12 p40 was changed after import homozygous gene fragment into cell [27]. It indicated that the change of allele might cause change in the expression of IL-12p40 and affect the function of IL-12p40. Then a series of immune responses were triggered. Finally, these events would lead to the onset of psoriasis. These findings prove that IL-12β rs3212227 may be the susceptibility gene of psoriasis. The result of this meta-analysis provided further evidence of the association betweenthe polymorphisms of IL-12β rs3212227 and psoriasis.
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It reported that the occurrence of psoriasis varied according to geographic region [2]. And the family genes are difference in each region. In this meta-analysis, subgroup analysis was performed by the difference of ethnicity. However, the subjects did not contain all the population. Thus, it proved that rs3212227 is the susceptibility gene of psoriasis in Asian and European. Further studies need to be done to study the influence of ethnicity.
Present study has some limitations that require specific consideration. The first one is that there is no enough data of age and sex to concern the influence of these confounding factors for the result of this meta-analysis. Second limitation is that the type of psoriasis cannot be analyzed because of the limited information. Furthermore, there are many other possible susceptibility genes, but only one of them was selected to do this meta-analysis.
Conclusions
In conclusion, we determined that there was significant association between the polymorphisms of IL-12β rs3212227 and psoriasis. IL-12β rs3212227 has a pivotal role in the pathogenesis of psoriasis. For researching the pathogenesis of psoriasis, all the susceptibility genes as well as the interaction among them need to be studied in the future.
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References
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2. Parisi R, Symmons DP, Griffiths CE, Ashcroft DM: Global epidemiology of psoriasis: a systematic review of incidence and prevalence. Journal of Investigative Dermatology 2012.
3. Naldi L: Risk Factors for Psoriasis. Current Dermatology Reports 2013, 2(1):58-65.
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6. Lamont AG, Adorini L: IL-12: a key cytokine in immune regulation. Immunology today 1996, 17(5):214-217.
7. Hong K, Chu A, Lúdvíksson BR, Berg EL, Ehrhardt RO: IL-12, independently of IFN-γ, plays a crucial role in the pathogenesis of a murine psoriasis-like skin disorder. The Journal of Immunology 1999, 162(12):7480-7491.
8. Tsunemi Y, Saeki H, Nakamura K, Sekiya T, Hirai K, Fujita H, Asano N, Kishimoto M, Tanida Y, Kakinuma T: Interleukin-12 p40 gene (IL12B) 3′-untranslated region polymorphism is associated with susceptibility to atopic dermatitis and psoriasis vulgaris. Journal of dermatological science 2002, 30(2):161-166.
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9. Clark MF, Baudouin SV: A systematic review of the quality of genetic association studies in human sepsis. Intensive care medicine 2006, 32(11):1706-1712.
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11. Lau J, Ioannidis JP, Schmid CH: Quantitative synthesis in systematic reviews. Annals of internal medicine 1997, 127(9):820-826.
12. Feng R-N, Zhao C, Sun C-H, Li Y: Meta-analysis of TNF 308 G/A polymorphism and type 2 diabetes mellitus. PloS one 2011, 6(4):e18480.
13. Liu ZH DY, Xiu LC, Pan HY, Liang Y, Zhong SQ, Liu WW, Rao SQ, Kong DL: A meta-analysis of the association between TNF-alpha -308G>A polymorphism and type 2 diabetes mellitus in Han Chinese population. PloS one 2013, 8(3):e59421.
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14. Capon F, Di Meglio P, Szaub J, Prescott NJ, Dunster C, Baumber L, Timms K, Gutin A, Abkevic V, Burden AD et al: Sequence variants in the genes for the interleukin-23 receptor (IL23R) and its ligand (IL12B) confer protection against psoriasis. Hum Genet 2007, 122(2):201-206.
15. Cargill M, Schrodi SJ, Chang M, Garcia VE, Brandon R, Callis KP, Matsunami N, Ardlie KG, Civello D, Catanese JJ et al: A large-scale genetic association study confirms IL12B and leads to the identification of IL23R as psoriasis-risk genes. American journal of human genetics 2007, 80(2):273-290.
16. Eiris N, Santos-Juanes J, Coto-Segura P, Gomez J, Alvarez V, Morales B, Queiro R, Diaz M, Corao AI, Lopez-Corte K et al: Resequencing of the IL12B gene in psoriasis patients with the rs6887695/rs3212227 risk genotypes. Cytokine 2012, 60(1):27-29.
17. Huffmeier U, Lascorz J, Bohm B, Lohmann J, Wendler J, Mossner R, Reich K, Traupe H, Kurrat W, Burkhardt H et al: Genetic variants of the IL-23R pathway: association with psoriatic arthritis and psoriasis vulgaris, but no specific risk factor for arthritis. The Journal of investigative dermatology 2009, 129(2):355-358.
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18. Nair RP, Ruether A, Stuart PE, Jenisch S, Tejasvi T, Hiremagalore R, Schreiber S, Kabelitz D, Lim HW, Voorhees JJ et al: Polymorphisms of the IL12B and IL23R genes are associated with psoriasis. The Journal of investigative dermatology 2008, 128(7):1653-1661.
19. Nair RP, Stuart PE, Kullavanijaya P, Kullavanijaya P, Tejasvi T, Voorhees JJ, Elder JT: Genetic evidence for involvement of the IL23 pathway in Thai psoriatics. Archives of dermatological research 2010, 302(2):139-143.
20. Oka A, Mabuchi T, Ikeda S, Terui T, Haida Y, Ozawa A, Yatsu K, Kulski JK, Inoko H: IL12B and IL23R gene SNPs in Japanese psoriasis. Immunogenetics 2013, 65(11):823-828.
21. Smith RL, Warren RB, Eyre S, Ho P, Ke X, Young HS, Griffiths CEM, Worthington J: Polymorphisms in the IL-12β and IL-23R Genes Are Associated with Psoriasis of Early Onset in a UK Cohort. Journal of Investigative Dermatology 2007, 128(5):1325-1327.
22. Zhu KJ, Zhu CY, Shi G, Fan YM: Meta-analysis of IL12B polymorphisms (rs3212227, rs6887695) with psoriasis and psoriatic arthritis. Rheumatology international 2013, 33(7):1785-1790.
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23. Jiqun C, Yating T, Jiawen L, Changzheng H, Zhixiang L, Daofan L: A study on the expression of interleukin (IL)-10 and IL-12 P35, P40 mRNA in the psoriatic lesions. Journal of Tongji Medical University 2001, 21(1):86-88.
24. Yawalkar N, Karlen S, Hunger R, Brand CU, Braathen LR: Expression of interleukin-12 is increased in psoriatic skin. Journal of investigative dermatology 1998, 111(6):1053-1057.
25. O’Neill JL, Kalb RE: Ustekinumab in the therapy of chronic plaque psoriasis. Biologics: targets & therapy 2009, 3:159.
26. Smith RL, Warren RB, Eyre S, Ho P, Ke X, Young HS, Griffiths CE, Worthington J: Polymorphisms in the IL-12β and IL-23R genes are associated with psoriasis of early onset in a UK cohort. Journal of Investigative Dermatology 2007, 128(5):1325-1327.
27. Morahan G, Huang D, Ymer SI, Cancilla MR, Stephen K, Dabadghao P, Werther G, Tait BD, Harrison LC, Colman PG: Linkage disequilibrium of a type 1 diabetes susceptibility locus with a regulatory IL12B allele. Nature genetics 2001, 27(2):218-221.
Table 1 Characteristics of included studies.
|
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Year |
Country |
population |
Experimental group/control group |
score |
PHWE How Do You Support Tight Deadlines?Urgent orders are prioritized with dedicated writers, ensuring quality delivery even within 3-6 hour timeframes. We thrive under pressure to meet your needs. Our rush-order specialists are trained to maintain excellence while working efficiently. Chat with support to confirm your deadline. Ace tutors specializing in urgent delivery maintain quality standards under pressure. |
||
|
mare（%） |
age (years) |
n |
||||||
|
Capon F1 |
2007 |
UK |
European |
65.4/50 Can You Include Primary Sources?Yes, we incorporate primary sources when requested, ensuring robust research and proper citation for academic rigor. We can also find credible sources if needed. Primary source integration strengthens arguments with authentic, firsthand evidence. Just specify your preferences in the order form. Research essay service includes primary source research for scholarly depth and credibility. |
52.1/- |
318/288 |
8 |
>0.05 |
|
Capon F2 |
2007 |
UK |
European |
42.4/50 |
44.1/49 What Is Your Quality Assurance Process?Every paper undergoes editing, plagiarism checks, and quality reviews to ensure it meets academic standards and your expectations. We leave no detail unchecked. Our multi-stage quality control includes subject experts who verify accuracy and depth. Your paper is guaranteed to impress. Paper writing quality passes through multiple expert review stages before delivery. |
519/528 |
8 |
>0.05 |
|
Cargill M1 |
2007 Can I Communicate Directly with My Writer?Yes, use our secure messaging system to discuss your order, share ideas, and get updates directly from your writer. This keeps you in the loop at every step. Direct communication ensures clarity and allows real-time collaboration on your project. Log in to your account to start chatting. Essay writer communication channels enable seamless collaboration throughout the writing process. |
USA |
European |
45.5 |
28 |
467/500 Do You Offer a Loyalty Program?Our loyalty program rewards repeat customers with discounts and perks, making each order more cost-effective. Save more with every paper you order. Accumulated points unlock exclusive benefits and priority service for returning clients. Check your account for your loyalty status and benefits. My assignment help becomes increasingly affordable through our generous loyalty rewards system. |
7 |
0.5876 |
|
Cargill M2 |
2007 Can You Help with Scholarship Essays?We craft persuasive scholarship essays, highlighting your achievements and goals to boost your applications impact. Our writers make your story stand out. Scholarship committees seek authentic narratives that demonstrate merit and potential. Share your aspirations in the order form for a winning essay. Essay helper expertise transforms scholarship applications into compelling funding opportunities. |
USA |
European |
45.5 |
29 |
498/498 |
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0.9129 |
|
Eiris N |
2012 |
Spain |
European |
54/55 |
47/47 |
304/422 |
6 |
0.1045 |
|
Hüffmeier U |
2009 |
Germany |
European |
62/58 |
48.2/31.6 |
1114/937 |
6 |
>0.05 |
|
Nair RP1 |
2008 |
Germany |
European |
– |
– |
360/1097 |
7 |
>0.05 |
|
Nair RP2 |
2008 |
USA |
European |
– |
– |
1450/1425 |
7 |
>0.05 |
|
Nair RP3 |
2010 |
Thailand |
Asian |
58/42 |
34/45 |
206/114 |
7 |
0.8488 |
|
Oka A |
2013 |
Japanese |
Asian |
– |
– |
560/560 |
8 |
– |
|
Smith RL |
2008 |
UK |
Mixed |
– |
– |
581/4681 |
6 |
0.5815 |
|
Tsunemi Y |
2002 |
Japanese |
Asian |
– |
– |
143/100 |
5 |
0.3177 |
PHWE，the result of the test of hardy-weinberg equilibrium
Table 2 Meta-analysis of the associations between IL-12β rs3212227 polymorphisms and psoriasis
|
Polymorphism |
population |
Test of association |
Test of heterogeneity |
|||
|
OR (95%CI) |
p |
P |
I2 |
|||
|
C vs. A |
Overall |
0.68 (0.64, 0.72) |
<0.01 |
0.18 |
27% |
|
|
European |
0.66 (0.61, 0.70) |
<0.01 |
||||
|
Asian |
0.71 (0.62, 0.82) |
<0.01 |
||||
|
Overall |
0.61 (0.53, 0.71) |
<0.01 |
0.02 |
57% |
||
|
European |
0.62 (0.52, 0.73) |
<0.01 |
||||
|
Asian |
0.45 (0.25, 0.82) |
<0.01 |
||||
|
CC vs. AC+AA |
Overall |
0.53 (0.43, 0.66) |
<0.01 |
0.85 |
0% |
|
|
European |
0.48 (0.36, 0.64) |
<0.01 |
||||
|
Asian |
0.56 (0.36, 0.85) |
<0.01 |
||||
|
CC vs. AA |
Overall |
0.46 (0.36, 0.57) |
<0.01 |
0.78 |
0% |
|
|
European |
0.42 (0.31, 0.56) |
<0.01 |
||||
|
Asian |
0.43 (0.26, 0.70) |
<0.01 |
||||
|
AC vs. AA |
Overall |
0.65 (0.59, 0.71) |
<0.01 |
0.16 |
33% |
|
|
European |
0.62(0.56, 0.69) |
<0.01 |
||||
|
Asian |
0.66 (0.44, 0.98) |
<0.01 |
Figure legends
Fig.1 Selection of relevant publications, reasons for exclusion.
Fig.2 Forest plot displaying the results of the meta-analysis on the genotype of C vs. A
Fig.3 Funnel plot analysis of publication bias.
________________________________________________________________________
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