Human Antibodies最新文献

Severe combined immunodeficiency (SCID) is a form of primary immunodeficiency disease (PID). It is characterized by a serious abnormality of the cellular and sometimes humoral system due to a deficiency in development of T cells, B cells and/or NK cells. The early diagnosis of SCID improves the prognosis. Typically, the initial consideration of SCID is made based on low lymphocyte counts. Notwithstanding, the heterogeneity of lymphocyte count presentation makes the diagnosis of SCID a significant challenge. The objective of this cross-sectional retrospective study was to analyze the lymphocyte subpopulation counts along with clinical manifestations within a Moroccan cohort diagnosed as SCID compared to children diagnosed with non-PID diseases. Thirty-five SCID confirmed patients were selected in the period between 2008 and 2018 and compared with non-PID patients. Results of peripheral blood T, B, and NK lymphocyte subpopulation counts were measured by flow cytometry for each SCID subtype. As expected, T cell count was less than 300 cells/μL in most patients with SCID (85.5%). Unexpectedly, significantly higher T cell counts were detected in some patients with a confirmed clinical diagnosis and family history of SCID. 5.7% of our SCID Moroccan cohort had T cell numbers in the range between 300 and 500 cells/μL. 8.7% of our SCID Moroccan cohort had T cell numbers higher than 500 cells/μL. Of the SCID subtypes, the proportion of SCID with B cell deficiencies was highly represented in our cohort. 71.4% of Moroccan SCID patients (25 out of 35 patients) were of T-B-subtype. Furthermore, 40% of the patients (14 out of 35 patients) had a T-B-NK+ profile and 31.4% had a T-B-NK- profile (11 out of 35 patients). The most common clinical manifestations observed in our SCID cohort were pneumonia, failure to thrive, candidiasis, diarrhea, bronchitis and urinary tract infections. Our results not only highlight the relatively frequent presence of atypical SCID in the Moroccan population with unexpectedly high T cell numbers, but also describes the incidence pattern of common SCID subtypes in Morocco. Physicians in Morocco may find this local region-specific difference in SCID important for making improved early diagnosis of this disease.

Background: One of the most severe side effects of solid-organ transplantation is posttransplant lymphoproliferative disease (PTLD). People with human immunodeficiency virus infection (HIV), an immunosuppressive disease comparable to HIV, have a higher chance of developing lymphoma when their peripheral blood contains elevated levels of the immunoglobulins kappa and lambda free light chains (FLCs).

Methods: This systematic review's objective was to monitor associated B lymphoma cells in PTLD patients. In order to find relevant studies published between 1/1/2000 and 1/9/2022, two independent researchers conducted searches (MT, AJ). A literature search of English language publications was conducted using MEDLINE through PubMed, EMBASETM through Ovid, the Cochrane Library, and Trip. In addition to Magiran and SID, we searched KoreaMed and LILACS for literature published in other languages. sFLC or PTLD, transplant, or Electrophoresis are terms used in the search strategy.

Results: A total of 174 studies were selected. After analyzing their correspondence with the required criteria, a final review of five studies was conducted. The manuscript presents current findings on the potential benefits of the clinical applicability of sFLCs in PTLD. While the preliminary results appear promising, the only consistent result is that early-onset PTLD is predicted within the first two years after transplant, a biomarker that could be used to diagnose the condition.

Conclusions: Therefore, PTLD has been predicted by using the sFLCs. There have been contradictory results to date. Future research could include assessing the quantity of sFLCs and their quality in transplant recipients. In addition to PTLD and complications after transplantation, sFLCs may provide insight into other diseases. To confirm the validity of sFLCs, more studies are needed.

Background: Interleukin (IL)-17 plays a central role in orchestrating the cytokine cascade and accelerates atherosclerosis and plaque vulnerability in animal models. However, epidemiological data evaluating the role of IL-17 levels in unstable angina are lacking. The aim of our study is to evaluate and compare the IL-17 levels in unstable angina (UA) cases before and after treatment.

Methods: This cross-sectional study was performed from July to October 2018 in Ali Iben-abitaleb heart center, Zahedan, Iran. 48 patients with UA in the age range of below 50 years entered the study. All demographic, past medical history, physical examination, electrocardiogram (EKG or ECG), and transthoracic echocardiogram (TTE) data were collected. Serum level of IL-17 was measured using enzyme-linked immunosorbent assay (ELISA) method. In all the tests, P< 0.05 was considered as statistically significant. All data analyses were performed using the SPSS 13.0 software (SPSS Inc., Chicago, Illinois, USA).

Results: In this study, 48 UA patients, including 34 women and 16 men with a mean age of 56.60 years were included in the study. The mean serum level of interleukin 17 after treatment (65.13 ± 53.29 pg/dl) was significantly lower than Its level before treatment (94.89 ± 51.25 pg/dL) (P< 0/05).

Conclusion: Our findings point towards a role of inflammation in the form of increased activity of IL-17 in UA patients and thus suggest that IL-17-driven inflammation may play a role in the promotion of clinical instability in patients with coronary artery disease.

There are many documents about benefits of exercise on human health. However, evidences indicate to positive effect of exercise on disease prevention, understanding of many aspects of this mechanism need more investigations. Determination of critical genes which effect human health.GSE156249 including 12 gene expression profiles of healthy individual biopsy from vastus lateralis muscle before and after 12-week combined exercise training intervention were extracted from gene expression omnibus (GEO) database. The significant DEGs were included in interactome unit by Cytoscape software and STRING database. The network was analyzed to find the central nodes subnetwork clusters. The nodes of prominent cluster were assessed via gene ontology by using ClueGO. Number of 8 significant DEGs and 100 first neighbors analyzed via network analysis. The network includes 2 clusters and COL3A1, BGN, and LOX were determined as central DEGs. The critical DEGs were involved in cancer prevention process.

The outbreak of the newly emerging severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) all over the world has caused global public health emergencies, international concern and economic crises. The systemic SARS-CoV-2 disease (COVID-19) can lead to death through causing unrestrained cytokines-storm and subsequent pulmonary shutdown among the elderly and patients with pre-existing comorbidities. Additionally, in comparison with poor nations without primary health care services, in developed countries with advanced healthcare system we can witness higher number of infections per one million people. In this review, we summarize the latest studies on genes associated with SARS-CoV-2 pathogenesis and propose possible mechanisms of the virus replication cycle and its triggered signaling pathways to encourage researchers to investigate genetic and immune profiles of the disease and try strategies for its treatment. Our review shows that immune response in people with different genetic background might vary as African and then Asian populations have lowest number of affected cases compared with European and American nations. Considering SARS-CoV-2 pathogenesis, we put forward some potentially important genetic gateways to COVID-19 infection including genes involved in the entry and replication of SARS-CoV-2 and the regulation of host immune response which might represent explanation for its spread, severity, and morality. Finally, we suggest that genetic alterations within these gateways could be critical factors in influencing geographical discrepancies of the virus, so it is essential to fully study them and design appropriated and reliable therapeutic agents against COVID-19.

Periodontal diseases are common conditions in almost all age groups and a public health problem. Numerous risk factors have been demonstrated for this condition. The main mechanism of tissue destruction in the periodontitis is the functional interactions between microbial pathogens and host immune responses, thus cytokines have crucial roles in the pathogenesis periodontitis. Our previous study has demonstrated the susceptibility role of HLA-DRB1*04 allele in development of this disease. So, the individuals who were positive for HLA-DRB1*04 allele were excluded. We aimed to appraise the function of cytokines in the pathogenesis of periodontitis via assessment of tissue and blood levels of a number of cytokine coding genes, namely IL-1B, CXCL8, IL-17, IFNG, TGFB and TNFA1. Expressions of IFNG, IL-17, TGFB and TNFA1 were significantly higher in the peripheral blood of individuals with periodontitis compared with unaffected persons (Posterior beta = 1.91, P value = 0.043; Posterior beta = 1.84, P value = 0.033; Posterior beta = 0.713, P value = 0.009 and Posterior beta = 2.85, P value = 0.001, respectively). Moreover, expression of IL-17 was higher in females compared with males (Posterior beta = 1.47, P value = 0.036). As the interaction effect between gender and group was remarkable for IL-17 expression, we further conducted subgroup analysis within gender group. Expression of IL-17 was higher in male patients compared with unaffected males (Posterior beta = 1.9, P value = 0.048). We did not detect any significant difference in the expression of these cytokines in tissues obtained from affected individuals and unaffected controls. Therefore, our results imply dysregulation of cytokine coding genes in patients with periodontitis and warrant further mechanistical studies.

Background: Morbidity and mortality associated with HIV infection is immune-mediated, and an understanding of HIV immunology will be beneficial in the management of HIV infectionOBJECTIVE: The objective of this research was to measure the levels of TNF-α, IL-6 and IFN-γ in asymptomatic HIV patients and non-HIV subjects, as well as their relationship with CD4 count.

Method: Blood samples were collected from 173 subjects, consisting of 125 asymptomatic HIV patients (44 HAART-naïve and 81 on HAART) and 48 non-HIV subjects. The IFN-, IL-6, and TNF- levels in the blood were determined using enzyme-linked immunosorbent assays, and the CD4 count of all participants was determined using flow cytometry.

Results: Regardless of treatment status, the IFN-γ levels of non-HIV subjects were significantly higher than those of HIV patients (p< 0.001). The opposite was true for IL-6, as the levels of IL-6 in non-HIV subjects were significantly lower than those in HAART-naïve HIV patients (p< 0.001) and those on HAART (p< 0.01). TNF-α levels did not differ between HIV patients and their non-HIV counterparts. Generally, the levels of these cytokines was not affected (p> 0.05) by immunosuppression (measured by CD4 count < 200 cells/μL) and there was no significant correlation between CD4 count and these cytokines (p> 0.05).

Conclusion: In conclusion, asymptomatic HIV infection decreased IFN-γ, increased IL-6, and had no effect on TNF-α levels, regardless of treatment status. Immunosuppression had no impact on these cytokine levels, and there was no relationship between them and CD4 counts.

Background: Little is known about the association between Human Immunodeficiency Virus (HIV) infection and risk of death among hospitalized COVID-19 patients. We aimed to investigate this association using a multicenter study.

Material and methods: This multicenter study was conducted using the registry database of Coronavirus Control Operations Headquarter from March 21, 2021 to January 18, 2020 in the province of Tehran, Iran. The interest outcome was COVID-19 death among hospitalized patients living with and without HIV. The Cox regression models with robust standard error were used to estimate the association between HIV infection and risk of COVID-19 death. The subgroup and interaction analysis were also performed in this study.

Results: 326052 patients with COVID-19 were included in the study, of whom 127 (0.04%) were living with HIV. COVID-19 patients with HIV were more likely to be female, older, and to have symptoms such as fever, muscular pain, dyspnea and cough. The death proportion due to COVID-19 was 18 (14.17%) and 21595 (6.63%) among HIV and non-HIV patients, respectively. Patients living with HIV had lower mean survival time compared to those without HIV (26.49 vs. 15.31 days, P-value = 0.047). Crude risk of COVID-19 death was higher among HIV patients than in non-HIV group (hazard ratio[HR]: 1.60, 1.08-2.37). Compared to those without HIV, higher risk of COVID-19 death was observed among patients with HIV after adjusting for sex (1.60, 1.08-2.36), comorbidities (1.49, 1.01-2.19), cancer (1.59, 1.08-2.33), and PO2 (1.68, 1.12-2.50). However, the risk of COVID-19 death was similar in patients with and without HIV after adjusting for age (1.46, 0.98-2.16) and ward (1.30, 0.89-1.89).

Conclusion: We found no strong evidence of association between HIV infection and higher risk of COVID-19 death among hospitalized patients. To determine the true impact of HIV on the risk of COVID-19 death, factors such as age, comorbidities, hospital ward, viral load, CD4 count, and antiretroviral treatment should be considered.