Human Antibodies最新文献

Background: Multiple Sclerosis known as MS, this chronic inflammatory demyelinating condition affects the nervous system. It is a heterogenic and multifactorial disease. The goal of the current study was to investigate the relationship between MS patients' IL18 gene expression and the vitamin D receptor gene polymorphism (FOK1rs2228570).

Objective: The aim of the study to investigate the association of vitamin D receptor (FOK1rs2228570) gene polymorphism and pro inflammatory cytokine (IL18) gene expression among multiple sclerosis Iraqi patients. Detection VDR polymorphism and determine whether this SNP is involved in susceptibility to multiple sclerosis and estimation IL18 gene expression and explore its relation with multiple sclerosis susceptibility.

Methods: Blood samples were taken from 75 MS patients in Iraq (30 men and 45 women), as well as from 75 volunteers who seemed to be in a favorable state of health and fell within the age range of 20 to 50 years. Tetra-ARMS Polymerase Chain Reaction (Tetra-ARMS PCR) was used to find polymorphisms in the vitamin D receptor (VDR) gene, and Real-time Polymerase Chain Reaction (RT-PCR) was used to measure IL18 gene expression.

Results: The findings from the analysis of VDR gene polymorphism in patients with MS indicated that the wild-type genotype T/T was present in 8 individuals, accounting for 10.6%, the heterogeneous genotype TC was 36 (48%), and the homogeneous genotype CC was 31 (41.3%), whilst T allele frequency was 52(34.6%) and C allele was 98(65.3%) with (P⩽ 0.01) significant difference and even as in control T/T genotype was 49(65.3%), TC genotype was 21(28%), CC genotype was 5(6.66%), T allele frequency was 119(79.3%) and C allele was 31(20.6%) with significant difference (P⩽ 0.001). While estimation of IL18 expression showed high elevation in patients' group (2.59 ± 0.51 fold) by significance difference (P⩽ 0.5) when compared to control group (1.35 ± 0.14 fold). The relationship between IL18 gene expression with VDR variant in MS patients demonstrated a significant rise (2.9 ± 0.51 fold) at CC genotype patients in IL18 folding gene expression, followed by (4.6 ± 0.17 fold) in TC genotype patients and finally (1.4 ± 0.08 fold) in TT genotype patients with highly significant (P⩽ 0.01).

Conclusion: The VDR(FOK1rs2228570) genotype was significantly correlated with IL18 expression in MS patients from Iraq.

Background: The correlation between dyslipidemia and the severity of coronavirus disease 2019 has been widely categorized. Dyslipidemia is one of the most dominant disorders among these patients. Systemic inflammation accompanied by cytokine storm hemostasis modifications and severe vasculitis have all been reported to occur among COVID-19 patients, and these may contribute to some severe complications.

Objective: The aim of this study is to assess the possible relationship between dyslipidemia and the severity of coronavirus disease 2019.

Methods: This work encompassed 200 patients with coronavirus disease 2019 (100 dyslipidemic and 100 normolipidemic) who were hospitalized at Baghdad Teaching Hospital/ Medical City-Baghdad, Iraq, from October 2021 to October 2022; their ages ranged between 40 and 55. Eligible individuals had a positive nasal swab polymerase chain reaction for severe acute respiratory syndrome coronavirus 2 infection. Every participant's anthropometric and clinical features were measured. The study includes the measurements of glycemic, lipid profile, renal function test, D-dimer, C-reactive protein, serum ferritin, and interleukin-6 in dyslipidemic and normolipidemic groups.

Results: Considerable increase (p= 0.001) in glycemic and lipid levels in the dyslipidemic group compared to normolipidemic. Moreover, dyslipidemic patients have higher lipid indices (ratios) than the normolipidemic group. Significant increases (p= 0.001) in serum urea and creatinine levels were found among the dyslipidemic group compared to normolipidemic. There was a non-considerable decrease (p= 0.062) in serum total protein in the dyslipidemic group concerning the normolipidemic. In contrast, a considerable decrease (p= 0.045) in serum albumin was detected in the dyslipidemic group compared to normolipidemic. D-dimer, serum C-reactive protein, ferritin, and interleukin-6 were significantly increased (p= 0.001) in the dyslipidemic group compared to normolipidemic.

Conclusion: Dyslipidemia potentially raises the severity of coronavirus disease 2019. There was a significant disturbance in renal function tests among coronavirus disease 2019 patients. The study found a significant and statistical difference in kidney functions between dyslipidemic and normolipidemic groups. The patients, especially the dyslipidemic ones, have experienced protein abnormalities and a significant inflammation rate reflected by higher C-reactive protein and interleukin-6, which is due to the severity of coronavirus disease 2019. It is possible to conduct more research with a larger sample size. The majority of people who have dyslipidemia need to be enlightened.

Background: Tuberculosis (TB) remains a universal health problem with significant morbidity and mortality. Understanding the genetic factors affecting TB susceptibility is crucial for effective prevention and treatment. Interleukin-10 (IL-10), a regulatory cytokine, may influence TB pathogenesis through genetic variations.

Methods: The PubMed, Embase, and Google Scholar databases were searched to find studies on the relationship between IL-10 gene variants and tuberculosis. Relevant studies from 2016 to 2024 were identified through database searches. The selected case-control studies met the inclusion criteria. Software such as Review Manager was used to analyze quantitative data, with statistical significance set at p< 0.05. We calculated odds ratios and their respective confidence intervals to evaluate the associations.

Results: Nine studies examined IL-10 gene polymorphisms (rs1800871 and rs1800872) in TB susceptibility. The present study did not show a notable association between IL-10 gene polymorphisms and TB among all genetic models (allelic, homozygote, heterozygote, dominant, and recessive). The obtained p-value > 0.05 indicates an insignificant association between both gene polymorphisms of IL-10. An OR-1.13; 95% CI-0.85, 1.50 was obtained for the SNP rs1800871, whereas an OR-1.02; 95% CI-0.75, 1.40 was obtained for the SNP rs1800872.

Conclusion: Our meta-analysis revealed no significant association between IL-10 gene polymorphisms and TB susceptibility, suggesting that these variations may not significantly contribute to TB susceptibility. Further research with a larger sample size and diverse ethnicities is needed to explore additional genetic variations and their implications in TB pathogenesis.

Background: Anti-mutated citrullinated vimentin (MCV) antibodies have recently been recommended as a better arthritis diagnostic marker.

Objectives: To investigate the association between anti-MCV antibodies and the clinical, functional, and radiographic characteristics of rheumatoid arthritis (RA) patients.

Methods: This case-control study was conducted on 40 RA patients and 40 healthy subjects. All patients were subjected to an assessment of disease using the 28-joint DAS (DAS28) and Clinical Disease Activity Index (CDAI), function by HAQ-DI, physical activity by International Physical Activity Questionnaire (IPAQ), fatigue by Functional Assessment of Chronic Illness Therapy (FACIT), serological tests as well as anti-MCV Abs measurement. A plain X-ray of both hands and wrists was done.

Results: The anti-MCV Abs level was significantly higher in RA patients than in healthy controls (P< 0.001). The anti-MCV Abs had a significant positive correlation with DAS, CDAI, HAQ, RF, Anti-CCP, and CRP (P= 0.006, 0.013, 0.005, < 0.001, < 0.001and 0.041 respectively) and a significant negative correlation with FACIT (p= 0.007). Positive anti-MCV RA patients had significantly higher erosions, JSN, and a total sharp score.

Conclusions: Anti-MCV Abs may contribute to poor physical activity and more fatigue in RA patients beyond their established role in disease activity and erosion.

Background: The advent of the Coronavirus Disease 2019 (COVID-19) has presented a substantial and urgent global public health issue. Biomarkers have the potential to be utilized for the identification of endothelium and/or alveolar epithelial damage in instances of COVID-19 infection.

Aim of the study: to evaluate the levels of Intercellular adhesion molecule-1 (ICAM-1) and Vascular cell adhesion molecule (VCAM-1) biomarkers in hospitalized patients who tested positive for COVID-19 infection using Polymerase Chain Reaction (PCR) with the virus specific Immunoglobulins; IgM, and IgG testing. This can help with improved clinical management and treatment programs.

Methods: A case-control study that involved 90 hospitalized patients who tested positive for COVID-19 and 40 apparently healthy control patients, subjects in both groups underwent nasopharyngeal swabs for PCR and blood sample collection for evaluation of serum; IgM, IgG, ICAM-1 and VCAM-1 levels.

Results: Males made up the vast majority of the patients (78.9%), with only a minor percentage of females (21.1%) P value 0.1641. Furthermore, every patient in this study had a minimum of one risk factor for COVID-19. The investigator's results show that COVID-19 patients had higher amounts of endothelial cell adhesion indicators (ICAM-1 and VCAM-1) with mean values of 126.27 ± 89.51 ng/mL and 109.74 ± 96.57 ng/mL respectively. While, ICAM-1 and VCAM-1, were present at normal levels in the control group with difference P value 0.0028 and 0.0032 in comparison to the patient's group respectively.

Conclusions: The adhesive markers ICAM and VCAM play a crucial role in the development of COVID-19 and the strong endothelial activation and dysfunction linked to both acute and persistent immunological responses is shown by the substantial correlation found in COVID-19 patients between the presence of IgM and IgG antibodies and higher levels of ICAM-1 and VCAM-1.

Background: The COVID-19 pandemic caused by SARS-CoV-2 is influenced by genetic and epigenetic factors, including miR-155, which affects immune cell and virus functions and laboratory biomarkers.

Objective: To evaluates miR-155's role as a biomarker for SARS-CoV-2 detection and monitoring, examining its significance in identifying infection in both vaccinated and unvaccinated individuals using ROC curve analysis.

Methods: Blood samples were collected from 70 patients who attended Medical City Hospital in Baghdad from June 2022 to April 2023 and were determined to be associated with SARS-CoV-2 (35 patients were hospitalized at the Intensive Care Units due to the severity of their symptoms while the other 35 were left in the hospital upon treatment.). Additionally, 35 samples were collected as a healthy control group.

Results: The expression level of miR-155 in the serum of samples showed a high level (fold change: 9.81 ± 5.50) in the severe patients' group in comparison with the moderate patients' group (fold change: 4.17 ± 2.93) and healthy group (fold change: 1.08 ± 0.01). To assess the performance of miR-155 and laboratory biomarkers, a (ROC) curve was utilized to determine the sensitivity and specificity.

Conclusions: The miR-155 gene, overexpressed in SARS-CoV-2 patients, correlates with disease activity and severity, potentially serving as a biomarker for diagnosis and a potential therapeutic target.

Background: Hepatitis A virus infection is a health threat with multiple transmission patterns across areas, It is evaluated using immune response markers IL-10 and IL-18, along with molecular and biochemical diagnostic methods for accurate diagnosis.

Objective: The association between liver damage and interleukin-10 and interleukin-18 levels in people with hepatitis A virus infection as indications of the risk of acute liver failure.

Methods: 110 samples were collected from Iraqi individuals from both sexes and different age groups ⩽ 1 to ⩾ 25, including 60 patients and 50 healthy people. All samples were collected from a hospital in Diwaniyah city, and the infection was confirmed by antiHAV IgM titers and One-Step RT-PCR. ELISA was used to determine the levels of IL-10 and IL-18, while Biochemical tests measured for alkaline phosphatase (ALP), alanine aminotransferase (ALT), aspartate aminotransferase (AST) and total serum Bilirubin (TSB) in serum.

Results: In this study, IL-10 levels were higher in HAV patients (0.12 ± 0.06 ng/L) compared to controls (0.11 ± 0.04 ng/L), but the difference was not significant (p= 0.17). Conversely, IL-18 levels were significantly elevated in patients (1.41 ± 0.71) versus controls (0.58 ± 0.35) (p= 0.00). Biochemical tests showed significantly elevated levels in HAV patients: ALT (170.18 ± 117.67 vs. 21.25 ± 7.41), AST (183.05 ± 128.13 vs. 26.00 ± 7.69), ALP (607.68 ± 214.93 vs. 202.02 ± 121.35), and TSB (2.77 ± 2.5 vs. 0.55 ± 0.14) (all p< 0.001). These findings underscore the potential of IL-10 and IL-18 as biomarkers for HAV severity and highlight their role in liver injury.

Conclusion: Our study highlights the important roles of IL-10 and IL-18 in acute hepatitis A and reveals their impact on the immune response and liver damage. Elevated levels of IL-10, IL-18 and Biochemical tests are associated with disease severity, suggesting their potential as biomarkers and therapeutic targets to improve the management of HAV infection.

Following infection and vaccination against SARS-CoV-2, humoral components of the adaptive immune system play a key role in protecting the host. Specifically, B cells generate high-affinity antibodies against various antigens of the virus. In this review, we discuss the mechanisms of immunity initiation through both natural infection and vaccination, shedding light on the activation of B cell subsets in response to SARS-CoV-2 infection and vaccination. The innate immune system serves as the initial line of primary and nonspecific defence against viruses. However, within several days following infection or a vaccine dose, a virus-specific immune response is initiated, primarily by B cells that produce antibodies. These antibodies contribute to the resolution of the disease. Subsequently, these B cells transition into memory B cells, which play a crucial role in providing long-term immunity against the virus. CD4+ T helper cells initiate a cascade, leading to B cell somatic hypermutation, germinal center memory B cells, and the production of neutralizing antibodies. B-cell dysfunction can worsen disease severity and reduce vaccine efficacy. Notably, individuals with B cell immunodeficiency show lower IL-6 production. Furthermore, this review delves into several aspects of immune responses, such as hybrid immunity, which has shown promise in boosting broad-spectrum protection. Cross-reactive immunity is under scrutiny as well, as pre-existing antibodies can offer protection against the disease. We also decipher breakthrough infection mechanisms, especially with the novel variants of the virus. Finally, we discuss some potential therapeutic solutions regarding B cells including convalescent plasma therapy, B-1 cells, B regulatory cell (Breg) modulation, and the use of neutralizing monoclonal antibodies in combating the infection. Ongoing research is crucial to grasp population immunity trends and assess the potential need for booster doses in maintaining effective immune responses against potential viral threats.

Introduction: Among the cancers that impacts men, prostate cancer considerably raises deaths for males around the world. Persons with tumours can have a localized or advanced form of the illness.

Objective: The present study aimed to determining the relationship between the level of cytokines (IL-10 and TNF-a) and PSA in the sera of patients and compared it with healthy.

Materials and methods: A case control study consist of three group included was in this study. The first group involves 50 patients with PC were observation in Al-Amal Oncology Hospital in the period from April 2021 to April 2022 under the supervision of oncology specialists was included in this study. Second group consist of 30 patients. They have benign hyper plaisa (BHP), this group has been collected from urosergical department . Third group was include 20 healthy volunteers (non prostate cancer and non BHP). Prostate specific antigen (PSA) was measured by mini - VIDAS device using kit supplied by Biomerieux - France. IL-10 and TNF-a levels were measured by ELISA technique using kit supplied by CAUSABIO - China.

Results: Results of the present study showed the 60-69 years age group scored highest percentage in benign (56.7%), malignant (54.0%), compared to control (healthy) (50.0%), while > 69 years scored least percentage in these groups (3.3%, 14.0%, and 25.0%) respectively with significant different (p< 0.05). Additionally, the IL-10 and PSA scored highest mean levels in the malignant group (1.22 ± 0.23 and 27.66 ± 6.31), while TNF-a scored highest mean levels in a benign group (0.30 ± 0.11). The least mean level of IL-10 was in healthy (0.42 ± 0.15), TNF-a in malignant (0.23 ± 0.03), and PSA in benign (6.73 ± 1.36). Finally, there is a significant difference among age groups and PSA, IL-10, and TNF-parameters.

Conclusions: We concluded the PSA, TNF-a and IL-10 parameters are play important roles in pathogenesis patients with prostate cancer. PCa is high prevalence in elderly population.