Xiaoqiang Wang; Yang Shen; Xia Ke; Suling Hong
Abstract
Background: T-helper 17 (Th17) cell response is engaged in the onset of allergic rhinitis (AR). Moreover, interleukin (IL)-38 is thought to be involved in inhibiting cytokine secretion in the Th17 pathway.Objective: To evaluate the regulatory function of IL-38 on abnormal Th17 responses in Chinese patients ...
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Background: T-helper 17 (Th17) cell response is engaged in the onset of allergic rhinitis (AR). Moreover, interleukin (IL)-38 is thought to be involved in inhibiting cytokine secretion in the Th17 pathway.Objective: To evaluate the regulatory function of IL-38 on abnormal Th17 responses in Chinese patients with AR.Methods: Forty-five participants, divided into an AR group (n=25) and a control group (n=20), were recruited for the study. In addition, the expression of IL-38 and Th17-related cytokines was measured as well as the Th17 cell count in participants. By implementing recombinant IL-38 (rIL-38), the intervention of human peripheral blood mononuclear cells (PBMCs) was performed. Then, flow cytometry, polymerase chain reaction (PCR), and enzyme-linked immunosorbent assay (ELISA) were used to detect theTh17 milieu.Results: The expression of IL-38 in the AR group notably reduced compared with that in the control, whereas Th17 cell frequency and the expression levels of its transcription factor (RORC) and cytokines (IL-17A and IL-23) increased. The differentiation and immune function of Th17 cells in PBMCs were inhibited by rIL-38.Conclusion: Th17 responses are inhibited by IL-38 in patients with AR. Therefore, the obtained findings indicate that IL-38 is a potential therapeutic target for Chinese patients with AR.
Moosa Rezwani; Abdulbaset Mazarzaei; Zahra Abbasi-Malati; Ali Akbar Pourfathollah
Abstract
Background: An issue that hinders researchers’ access to Natural Killer (NK) cells is their low proportion in peripheral blood leukocytes. This issue is currently addressed by methods involving a series of differentiation and expansions that are time-consuming and expensive.Objective: We have investigated ...
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Background: An issue that hinders researchers’ access to Natural Killer (NK) cells is their low proportion in peripheral blood leukocytes. This issue is currently addressed by methods involving a series of differentiation and expansions that are time-consuming and expensive.Objective: We have investigated whether the used leukocyte reduction filters, a by-product in the blood transfusion practice that currently is considered waste, can be utilized as a source of the NK cells.Methods: Following the blood donation of 46 donors based on the Iranian Blood Transfusion Organization’s protocols, a sample of peripheral blood of each donor and the leukocyte reduction filter used in their donation procedure have been obtained. The entrapped cells were flushed back from the leukocyte reduction filters. Both groups of samples were analyzed using an automatic hematological analyzer. NK cell isolation was done by the MACS negative selection method. The samples have been comparatively analyzed utilizing flow cytometry data of NK cells’ subpopulation compositions, viability, degranulation patterns, and cytotoxic capacity against the K562 cell line.Results: Every major leukocyte population was abundant in the samples extracted from the used leukocyte reduction filters. The NK cells extracted from leukocyte reduction filters did not show any statistically meaningful differences (P<0.5) from peripheral blood samples in terms of subpopulation composition, viability, degranulation potency, and cytotoxic capacity.Conclusion: Used leukocyte reduction filters can be considered an economic, easy to obtain, and robust source of abundant research-grade NK cells.
Mohammad Jafar Mahmoudi; Maryam Mahmoudi; Fereydoon Siassi; Fazel Shokri; Mohammad Reza Eshraghian; Amir Hassan Zamani; Reza Chahardoli; Mona Hedayat; Jalal Khoshnoodi; Hashem Nayeri; Nima Rezaei; Ali-Akbar Saboor-Yaraghi
Volume 8, Issue 1 , March 2011, , Pages 27-33
Abstract
Background: Atherosclerosis, a chronic inflammatory disease of the vessel wall is characterized by local and systemic immune responses to a variety of antigens. Oxidized low-density lipoprotein (oxLDL) is considered as an important determining factor in the pathogenesis of atherosclerosis. Objective: ...
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Background: Atherosclerosis, a chronic inflammatory disease of the vessel wall is characterized by local and systemic immune responses to a variety of antigens. Oxidized low-density lipoprotein (oxLDL) is considered as an important determining factor in the pathogenesis of atherosclerosis. Objective: The purpose of this study was to investigate the degree of peripheral blood mononuclear cells (PBMC) vulnerability to in vitro oxLDL-induced cytotoxicity from atherosclerotic patients in comparison to healthy individuals. Methods: Thirty patients with atherosclerotic lesions, confirmed by angiography, and 30 matched healthy individuals were investigated. PBMC was prepared from individuals' blood samples which were further stimulated with low dose (1 μg/mL) and high dose (50 μg/mL) of extensively oxidized LDL. MTT assay was utilized to measure cell viability and proliferation. Stimulation index (SI) was calculated as mean ratio of optical density (OD) of the stimulated cells divided by OD of untreated cells. Results: Low dose oxLDL treatment caused no significant proliferative or cytotoxic effect in the control group; however, similar treatment caused significant cytotoxic effect in the patient group compared to the controls (p=0.026). High dose oxLDL treatment induced more significant cytotoxicity in the patient compared to the control group (p=0.006). Comparison of the SI between the two groups of patients and controls showed significantly lower index by either the low (p=0.03) or the high dose (p<0.001) oxLDL in the patients compared to the controls. Conclusions: PBMC from patients with atherosclerosis showed increased susceptibility to oxLDL-induced cytotoxicity. Our results imply that prolonged exposure to elevated levels of circulating oxLDL could weaken the cellular defense mechanisms by progressive depletion of the pool of antiapoptotic proteins, rendering the cells more vulnerable to oxLDL-induced cell death.