The recent study assessed TGF-β and IL-10 as immunosuppressive cytokines of the cell
mediated immunity (CMI) against Brucella in the serum of some brucellosis patients.
Serum from 15 patients and 15 healthy individuals were obtained, and then cytokine
concentrations above were investigated. Concentrations of TGF-β induced in the serum of
acute patients (89.73 ± 15.55 ng/ml) were higher than healthy group (58.86 ± 17.89 ng/ml,
P < 0.0001). While, no significant differences were found in the concentration of IL-10
between two groups. Based upon the findings of our study, the contribution of these
cytokines to the pathobiology of infection had been shown. Therefore, assessment of
immunosuppressive cytokines as TGF-β and IL-10 levels may be a potential diagnostic
strategy for patients with brucellosis.
M. Mirzakhani, M. Shahbazi, S. Darvish and Mousa Mohammadnia-Afrouzi
Background: Lymphocytes proliferate considerably following appropriate stimulation in vitro. Autologous T cells are obtained from whole blood or tissue sites in relatively limited amounts. We need a method to expand these cells efficiently, study their functions and manipulate them to create appropriate cells for transferring to the patient with infection and cancer. Objectives: The aim of this study is to determine proliferation ability of two different stimulators on CD4+ lymphocytes. Methods: Lymphocytes were isolated from blood samples of healthy donors after removing adherent cells (monocytes).The efficacy of MACSiBead™ coated with anti-CD2, anti-CD3, anti-CD28 (anti-CD2/CD3/CD28) was compared with Phytohaemagglutinin A (PHA) on CD4+ lymphocytes proliferation using carboxyfluorescein diacetate succinimidyl ester (CFSE) in cell culture media. The percentage of proliferating cells was analyzed using flow cytometry. Results: Both stimulators induced extensive proliferation of CD4+ lymphocytes but proliferation ability of PHA was higher compared to stimulation by anti-CD2/CD3/CD28 MACSiBead™. The proliferation rate of cells stimulated by PHA was 93.8% ± 3.37% whereas it was 85.2% ± 4.7% in cells stimulated by anti-CD2/CD3/CD28 MACSiBead™. Conclusions: Our results show that MACSiBead™ along with PHA can be used to obtain a large number of expanded CD4+ lymphocytes.
Ali Khalili, Soheil Ebrahimpour, Iradj Maleki, Saeid Abediankenari and Mousa Mohammadnia Afrouzi
Background. Regulatory T (Treg) cell plays a key role in autoimmune diseases. We evaluated the regulatory function and frequency of Treg cells and secreted IL-10, IL-35 concentration in Crohn’s disease (CD).
Methods. Twenty-three patients with CD and 25 healthy controls (HC) were included in this study. We analysed the alteration of Tregs frequency using flow cytometry for CD4, CD25, CD127 and FoxP3 markers. Surface expression of CD4, CD25 and CD127 markers were used for isolation of relatively pure Treg cells. Suppressive activity of Tregs was determined by measuring their ability to inhibit the proliferation of T responder (Tres) cells. In addition, the amounts of IL-10 and IL-35 cytokines in co-culture supernatants were measured by ELISA assay after stimulation with anti-CD2/CD3/CD28.
Results. CD patients had significantly lower frequency of CD4+ CD25+ CD127low FoxP3+ Treg cells in comparison with controls (2.17 ± 1.04 vs. 2.83 ± 1.07, p = 0.0352). Additionally, Treg cells mediated suppression was not significantly different in CD patients compared to controls. There was a significant difference in IL-10 secretion in response to anti-CD2/CD3/CD28 stimulation compared with HC (p = 0.0074).
Conclusion. The frequency of CD4+ CD25+ CD127low FoxP3+ Tregs decreased in active stage of CD but there was no impaired suppressive function of CD4+ CD25+ CD127low FoxP3+ Treg cells. We suggest that an alteration in the balance of Tregs and T effectors may contribute to pathogenesis of CD.
Guillain–Barré syndrome (GBS) is an inflammatory disorder and an acute immune-mediated demyelinating neuropathy that causes reduced signal transmissions, progressive muscle weakness, and paralysis. The etiology of the syndrome still remains controversial and uncertain. GBS can be initiated and triggered by respiratory tract infections such as influenza, and intestinal infections such as Campylobacter jejuni. In addition, there is considerable evidence suggesting links between influenza vaccination and GBS. As reported previously, the incidence of GBS in individuals receiving swine flu vaccine was about one to two cases per million. Despite the influenza vaccine efficacy, its association with an immune-mediated demyelinating process can be challenging as millions of people get vaccinated every year. In this review we will discuss the association between influenza infection and vaccination with GBS by focusing on the possible immunopathological mechanisms.