Quercetin is a naturally occurring polyphenol flavonoid which is rich in antioxidants. It has anti-allergic functions that are known for inhibiting histamine production and pro-inflammatory mediators. Quercetin can regulate the Th1/ Th2 stability, and decrease the antigen-specific IgE antibody releasing by B cells. Quercetin has a main role in antiinflammatory and immunomodulatory function which makes it proper for the management of different diseases. Allergic diseases are a big concern and have high health care costs. In addition, the use of current therapies such as ß2-agonists and corticosteroids has been limited for long term use due to their numerous side effects. Since the effect of quercetin on allergic diseases has been widely studied, in the current article, we review the effect of quercetin on allergic diseases, such as allergic asthma, allergic rhinitis (AR), and atopic dermatitis (AD).

Coronavirus disease 2019 (COVID-19), an acute respiratory infection, is largely associated with dysregulation and impairment of the immune system. This study investigated how the immune system changes were related to disease severity in COVID-19 patients. The frequencies of different immune cells and levels of pro- and anti-inflammatory cytokines in whole blood of participants were determined by flow cytometry and enzyme-linked immunosorbent assay, respectively. The values of other inflammatory agents were also studied. In the late recovery stage, unlike CD56high CD16+/− NK cells and monocytes, CD56low CD16+ NK cell numbers were increased ( P < 0.0001–0.05). Th1, Th2, and Th17 cell percentages were significantly lower in patients than healthy control ( P < 0.0001–0.05), while their frequencies were increased following disease recovery ( P < 0.0001–0.05). The numbers of Tregs, activated CD4+ T cells, and exhausted CD8+ T cells were significantly decreased during a recovery ( P < 0.0001–0.05). No significant change was observed in exhausted CD4+ T cell number during a recovery ( P > 0.05). B cell showed an increased percentage in patients compared to healthy subjects ( P < 0.0001–0.05), whereas its number was reduced following recovery ( P < 0.0001–0.05). IL-1α, IL-1β, IL-6, TNF-α, and IL-10 levels were significantly decreased in the late recovery stage ( P < 0.0001–0.05). However, TGF-β1 level was not significantly changed during the recovery ( P > 0.05). Lymphocyte numbers in patients were significantly decreased ( P < 0.001), unlike ESR value ( P < 0.001). Lymphocyte number was negatively correlated to ESR value and Th2 number ( P < 0.05), while its association with monocyte was significantly positive at the first day of recovery ( P < 0.05). The immune system changes during the disease recovery to improve and regulate immune responses and thereby may associate with the reduction in disease severity.

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BackgroundAutism is a disease of complex nature with a significant genetic component. The importance of renin-angiotensin system (RAS) elements in cognition and behavior besides the interaction of angiotensin II (Ang II), the main product of angiotensin-converting enzyme (ACE), with neurotransmitters in CNS, especially dopamine, proposes the involvement of RAS in autism. Since the genetic architecture of autism has remained elusive, here we postulated that genetic variations in RAS are associated with autism.MethodsConsidering the relation between the three polymorphisms of ACE (I/D, rs4343 and rs4291) with the level of ACE activity, we have investigated this association with autism, in a case-control study. Genotype and allele frequencies of polymorphisms were determined in DNAs extracted from venous blood of 120 autistic patients and their age and sex-matched healthy controls, using polymerase chain reaction (PCR) and PCR–restriction fragment length polymorphism (PCR–RFLP) methods.ResultsThere were strong associations between both DD genotype of ACE I/D and the D allele, with autism (P = 0.006, OR = 2.9, 95% CI = 1.64–5.13 and P = 0.006, OR = 2.18, 95% CI = 1.37–3.48 respectively). Furthermore, a significant association between the G allele of rs4343 and autism was observed (P = 0.006, OR = 1.84, 95%CI = 1.26–2.67). Moreover, haplotype analysis revealed an association between DTG haplotype and autism (P = 0.008).ConclusionOur data suggests the involvement of RAS genetic diversity in increasing the risk of autism.

The failure of immunological tolerance to self‐antigens plays a fundamental role in the pathogenesis of systemic lupus erythematosus (SLE). PD‐1 is an inhibitory receptor for regulating the immune system and preventing development of autoimmune disorders. This study aimed to determine the role of four single‐nucleotide polymorphisms (SNPs) within programmed cell death 1 (PDCD1 or PD‐1) gene and haplotypes defined by these SNPs in susceptibility to SLE in the Iranian population. Blood samples were obtained from 253 SLE and 564 healthy subjects. Red blood cells were lysed and genomic DNAs were extracted using salting‐out method. Genotype determinations of PD1.1, PD1.3, PD1.5 and PD1.9 SNPs were performed by polymerase chain reaction–restriction fragment length polymorphism (PCR‐RFLP), and 12 haplotypes were constructed by PDCD1 SNPs. Our results showed significant differences in PD1.5 genotype frequencies between patient and control groups (p < .001). The frequencies of PD1.5 C/C, C/T and T/T genotypes versus other genotypes in SLE patients significantly differed from healthy subjects (p < .001, p = .001 and p = .002, respectively). Allelic analysis indicated a significant association between the frequency of PD1.5C allele and development of SLE in our population (odds ratio [OR] = 1.91, 95% confidence interval [CI] = 1.51–2.42, p < .001). At the haplotype level, GGCC, GACT and GGCT haplotypes were significantly different between SLE and control groups (OR = 2.14, 95% CI = 1.73–2.66, p < .001; OR = 9.76, 95% CI = 4.47–21.3, p < .001; and OR = 0.32, 95% CI = 0.24–0.42, p < .001, respectively). Based on these findings, PD1.5 SNP and some haplotypes of PDCD1 contribute to SLE risk in the Iranian population.

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Environmental and genetic factors play a fundamental role in the pathogenesis of basal cell carcinoma (BCC) defined as the most common cancer of skin. Programmed death‐1 (PD‐1), encoded by programmed cell death‐1 (PDCD1) gene, serves as an inhibitory molecule in the suppression of immune responses and a risk factor in the development of different cancers. In this study, we investigated the role of two single nucleotide polymorphisms (SNPs) within PDCD1 gene, and haplotypes defined by these SNPs, in the development of BCC in an Iranian population. Whole blood samples were obtained from 210 BCC and 320 healthy subjects. Genomic DNA was extracted from whole blood samples, polymerase chain reaction‐restriction fragment length polymorphism (PCR‐RFLP) was used to genotype determinations of PD1.3 (rs11568821) and PD1.5 (rs2227981) SNPs, and 4 haplotypes were constructed by PDCD1 SNPs. The frequency of G allele of PD1.3 was significantly higher in BCC patients than healthy subjects (p < 0.02), while these significant differences were not observed in the frequencies of PD1.5 alleles between BCC and healthy subjects. Moreover, we found that there were no statistically significant differences in PD1.3 and PD1.5 genotypes between BCC and control groups. Of all estimated haplotypes for PDCD1, only AC haplotype was associated with BCC (OR = 0.22, 95% CI = 0.06–0.79, p < 0.01). These findings suggest that PD1.3G allele and AC haplotype of PDCD1 contribute to BCC in the Iranian population. However, further studies in different populations with larger sample size are required to confirm this study.

Background: Asthma is a chronic and complex inflammatory disease of the respiratory tract. Also, multiple sclerosis (MS) is a chronic inflammatory demyelinating disease of the central nervous system. Against this background, IL-33 and IL1RL1 play a critical role in autoimmune and inflammatory disorders. Here, we explored the IL-33 serum level and two potential genetic variants in the IL33 gene and its receptor in Iranian asthma and MS patients. Results: The level of IL33 was significantly higher in asthma and MS patients compared to the control group (P< 0.001- P<0.001).The frequency distribution of the genotype in rs1342326 variant of IL-33 gene in patients with asthma, MS and healthy subjects was not significantly different (P>0.05). The frequency distribution of the genotype in rs10204137 variant of IL-33 gene in MS patients and healthy subjects was significantly different (p = 0.013). Methods: This study consisted of asthma (n=140) and MS patients (n=140), and healthy subjects (n=72). Genotyping was carried out in two genetic polymorphisms, rs1342326 variant of IL-33 and rs10204137SNP variant of IL-33 receptor genes, using High- Resolution Melt Real- Time PCR based method. The level of serum IL-33 was also measured using enzyme-linked immunosorbent assay method. Conclusion: Our findings demonstrated that asthma and MS patients had a higher level of IL-33, and IL-33 receptor genetic polymorphism was associated with MS. Further studies in a larger multicenter setting are needed to explore the value of this marker as a risk stratification biomarker.