2022 Impact Factor: 1.5
2023 CiteScore: 2.6
pISSN: 1735-1502
eISSN: 1735-5249
Chairman:
Mostafa Moin, M.D.
Editors-in-Chief:
Masoud Movahedi, M.D.
Vol 9, No 3 (2010)
Atherosclerosis is a chronic inflammatory disease of the arterial wall characterized by innate and adaptive immune responses to a variety of microbial and self-antigens. Given the crucial role of adaptive immunity in the pathogenesis of atherosclerosis, this study was performed to investigate the proliferative response of peripheral blood mononuclear cells (PBMC) and interleukin (IL)-2 production in patients with coronary artery disease (CAD).
In this study, 25 patients with chronic stable CAD and 25 healthy individuals were investigated. The PBMCs were separated and stimulated with phytohaemagglutinin (PHA). MTT assay was performed to measure cell viability and proliferation. IL-2 concentrations in cell culture supernatants were determined by Enzyme-Linked Immunosorbent Assay.
PHA-stimulated cells revealed a significantly increased optical density (OD) in both groups of patients (p=0.004) and controls (p<0.001). However, the patient group showed a significantly lower Stimulation index (SI) (p=0.001). Upon in vitro stimulation with PHA, IL-2 levels were significantly increased in both groups of patients and controls (p<0.001). However, IL-2 concentrations were significantly lower in the patient group (p=0.018). Six patients showed defective IL-2 production, whereas similar finding was not observed in the normal control subjects (p=0.022). PBMCs from patients with coronary artery disease showed defective PHA-induced mitogenesis and IL-2 production.
Considering the autoimmune nature of atherosclerosis, decreased IL-2 production may potentially enhance the atherogenic process, leading to spontaneous activation of autoreactive T lymphocytes.
Blocking antibodies are valuable tools for inhibiting the specific receptor- ligand interactions. The interaction of co-stimulatory molecules on the antigen presenting cells with their ligands on T cells is an essential step for T cell activation. In the present study, the effect of blocking antibody against CD40 on its T cell stimulatory potential is investigated.
The DCs (dendritic cells) were collected from the mice spleens and then cultured in vitro. We used purified rat anti-mice CD40 (Clone HM40-3) (BD USA) as a blocking antibody and the appropriate titer of the blocking antibody was determined by flow cytometry. The DCs were then treated by antibody and used in MLR assay.
The results of these experiments showed that CD40 blockade were associated with the increase in the of IL-4 secretion, shifting the DCs to stimulate Th2 cytokine production by the allogenic T cells, while the secretion of IL-12 by DCs decreased. Similarly, the DCs with reduced CD40 expression poorly responded to alloantigen stimulation in the MLR.
Collectively, these results emphasize the importance of CD40 pathway in tolerogenic DCs generation and also support the idea that downregulation of CD40 is effective in inhibiting the allostimulatory function.
Galactomannan (GM) antigen is an aspergillus specific antigen that is released during the growth phase of invasive aspergillosis. We aimed to find the optimum cut-off and accuracy of serum Galactomannan assay in immunocompromised patients.
Immunocompromised patients diagnosed with invasive pulmonary aspergillosis (IPA) based on the European Organization for Research and Treatment of Cancer/Invasive Mycosis Study Group (EORTC/MSG) with three levels of certainty proven, probable and possible, referred for GM antigen measurement at Immunology, Asthma and Allergy Research Institute (IAARI) from 2006 to 2009 and if they met the criteria were enrolled in this study.
Totally 49 patients with IPA were enrolled in our study. According to EORTC/MSG, patients categorized into three levels of certainty: They were diagnosed as ‘proven' invasive pulmonary aspergillosis 16(32.7%), ‘probable' 18(36.7%) and ‘possible' 15(30.6%). The most common host risk factor was solid tumors 17(34.7%). The accuracy of Galactomannan assay increased from 0.5 to 2 cut-offs. The optimum sensitivity and specificity obtained at the index cut-off of ≥1.5 for diagnosis of "proven" IPA; which were respectively, 69.2% and 72.2%. Other cut-offs had high variance between sensitivity and specificity for diagnosis of IPA.
The calculated cut-off gained by receiver operating characteristic (ROC) analysis for detecting proven IPA was 1.5. Intermediate accuracy of serum GM test in conjunct with clinical findings would help early IPA detection among immunocompromised patients.
Celiac disease has been associated with other autoimmune disorders such as autoimmune hepatitis, moreover it is known that T cell mediated immune response to dietary gluten and released cytokines are important for the entheropathy seen in celiac disease. We investigated celiac autoantibodies in patients with autoimmune hepatitis (AIH), and chronic hepatitis B (CHB).
Sera from 84 patients with Autoimmune Hepatitis (AIH) type 1 and 88 patients with Chronic Hepatitis B (CHB) were tested for Immunoglobulin A and G antibodies to Gliadin, Immunoglobulin A antibodies to tissue transglutaminase using enzyme immunoassay, and Immunoglobulin A anti-endomysial antibodies by both indirect immunofluorescence, and enzyme immunoassay. The patients positive for anti-endomysial antibodies and/or anti tissue transglutaminase antibodies were considered for deuodenal biopsy. The study was approved by Research Center for Gastroenterology and Liver Disease Ethics Committee and all patients gave their written informed consent to participate.
Immunoglobulin A anti-endomysial and Immunoglobulin A anti-gliadin antibodies were positive in two out of 84 patients with AIH. Moreover, Immunoglobulin A anti-gliadin antibodies were positive in another patient who was also positive for anti tissue transglutaminase antibodies. Tissue transglutaminase antibodies were positive in eight (9.1%) of 88 patients with CHB, two of which were also positive for anti-endomysial antibodies. One of the patients with CHB was only positive for anti-endomysial antibodies.
Compared with the general population, the prevalence of celiac autoantibodies in CHB and AIH patients is relatively high, and it is noteworthy that most positive patients were asymptomatic for celiac disease. We suggest screening for celiac disease before and during treatment in patients with viral and autoimmune hepatitis.
Asthma is one of the most common chronic diseases of childhood. Inhaled corticosteroids (ICS) are the recommended controller drug for asthma treatment.
The aim of our study was to determine concerns and fears of parents of children with asthma towards the use of ICS. One hundred parents of asthmatic children were interviewed using structural questionnaire.
Airway inflammation was reported by only 6% of interviewed parents, whereas airway narrowing was addressed by 34%. Interesting data, 71% of parents were concerned with the role of steroids in asthma treatment, but more than half (53%) of them addressed fears from side effects. Apparent gaps were found in knowledge of parents of asthmatic children about ICS as controller asthma medication. So, physician and health providers should explain to asthmatic parents that airway inflammation is the core for asthma management. This may remove fears about ICS and thus improve adherence to treatment.
Nicotine is one the chemical substance with high level of toxically. It crosses the placenta and accumulates in the developing organs of fetus. Our previous investigations indicated that collagen type IV plays a key role in basement membrane of various embryonic organs. In this study we evaluated the effect of maternal nicotine exposure pre and postnatal period on collagen IV expression during bronchogenesis and alveolarization in the lungs of newborn mice. Female Balb/C mice were mated and Sperm positive in vaginal smear was designated as embryonic day zero. Pregnant mice were divided into 2 experimental and 2 control groups.
Experimental group 1, received 3 mg/kg nicotine intrapritoneally from day 5 of gestation to last day of pregnancy. Experimental group 2 received the same amount of nicotine during the same gestational days as well as 2 first week after birth (lactation). The control groups received the same volume of normal saline during the same periods. At the end of exposure times, all of newborns were anesthetized and their lungs were removed for immunohistochemical method.
Our finding indicated that collagen reaction in the bronchial basement membrane and extra cellular matrix of lung parenchyma in experimental groups increased significantly compared to control groups. Our results also showed alveolar remodeling and abnormal bronchogenesis were observed in experimental group especially group 2.
These data indicate that maternal nicotine exposure may induce abnormal collagen IV expression and cause defects in bronchopulmonary development.
A study was done about non-participation during Phase III of the International Study of Asthma and Allergy in Childhood (ISAAC III) in Valencia to determine whether the non-response rate significantly affected the results obtained in Valencia. Of the schools selected to participate in ISAAC III, 13.3% denied not to, the main reason being they were already participated in a similar study. The ISAAC III questionnaire was handed out to participating schools for the parents of 6,358 schoolchildren aged 6-7 years. Of these, 53.4% responded correctly.
The remaining 46.6% were given a non-response questionnaire (NRQ), of which 4.1% completed the questionnaire correctly. The main reason why parents who received the NRQ did not participate in ISAAC III was that their children had neither asthma nor other atopic disease, so interest was null. No significant statistical differences were observed between the prevalence of asthma in the schoolchildren who participated in ISAAC III and in the non-participants who answered the NRQ. These results suggest that the ISAAC III results relating to asthma are not biased by non-response.
Autoimmune lymphoproliferative syndrome (ALPS) is an uncommon nonmalignant lymphoproliferative disease which is characterized by chronic, persistent or recurrent lymphadenopathy, splenomegaly, hepatomegaly, immune cytopenia, hypergammaglobinemia and increased risk of lymphoma.
We report a 2-year old boy with hepatosplenomegaly as first presentation. Petechial and purpuric rashes with massive cervical lymphadenopathies developed 10 months later. In laboratory tests anemia, thrombocytopenia and hypergammaglobinemia were observed. According to flocytometry increased double negative T cells and by apoptosis assay decrease apoptosis of lymphocytes accompanied clinical manifestations, thus diagnosis of ALPS was established.
In conclusion; in all patients with massive lymphadenopathy and hepatosplenomegay; especially with cytopenia; ALPS should be considered.
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