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Dendritic Cell Stimulation by IFN-β Alters T Cell Function via Modulation of Cytokine Secretion in Diabetes Type 1
Abediankenari Saeid,Ghasemi Maryam,Eslami Mohammad Bagher
Acta Medica Iranica , 2009,
Abstract: During antigen capture and processing, mature dendritic cells (DC) express large amounts of peptide-MHC complexes and accessory molecules on their surface. We investigated the role of IFN-β in induction HLA-G expression on the monocyte derived DC and cytokine profile in diabetes type 1. We accomplished secretary pattern and total cytokine production of the Th1 cytokine (IL-2, γIFN) and Th2 cytokines (IL-4, IL-10) before and after mixed leukocyte reaction (MLR) of 30 diabetic patients and 30 normal subjects. In this study a significant increase of IL-10 and γIFN reduction after IFN-β Therapy in culture in presence of HLA-G bearing DC as compared to control were seen. It is seen that dendritic cell causes IL-10 production of T cell in vitro that reduce T cell activation from diabetes patients and normal subjects resulted to the production and expression of HLA-G on these cells from both groups. Using mixed leukocyte reaction, it was found that IFN-β-treated dendritic cell mediated the inhibition of autologous T cell activation via IL-10 production and level of HLA-G on dendritic cell may be correlated to disease activity in diabetes patients and it could also serve as a useful marker for disease progress and treatment.
AMP Affects Intracellular Ca2+ Signaling, Migration, Cytokine Secretion and T Cell Priming Capacity of Dendritic Cells  [PDF]
Elisabeth Panther, Thorsten Dürk, Davide Ferrari, Francesco Di Virgilio, Melanie Grimm, Stephan Sorichter, Sanja Cicko, Yared Herouy, Johannes Norgauer, Marco Idzko, Tobias Müller
PLOS ONE , 2012, DOI: 10.1371/journal.pone.0037560
Abstract: The nucleotide adenosine-5′-monophosphate (AMP) can be released by various cell types and has been shown to elicit different cellular responses. In the extracellular space AMP is dephosphorylated to the nucleoside adenosine which can then bind to adenosine receptors. However, it has been shown that AMP can also activate A1 and A2a receptors directly. Here we show that AMP is a potent modulator of mouse and human dendritic cell (DC) function. AMP increased intracellular Ca2+ concentration in a time and dose dependent manner. Furthermore, AMP stimulated actin-polymerization in human DCs and induced migration of immature human and bone marrow derived mouse DCs, both via direct activation of A1 receptors. AMP strongly inhibited secretion of TNF-α and IL-12p70, while it enhanced production of IL-10 both via activation of A2a receptors. Consequently, DCs matured in the presence of AMP and co-cultivated with naive CD4+CD45RA+ T cells inhibited IFN-γ production whereas secretion of IL-5 and IL-13 was up-regulated. An enhancement of Th2-driven immune response could also be observed when OVA-pulsed murine DCs were pretreated with AMP prior to co-culture with OVA-transgenic na?ve OTII T cells. An effect due to the enzymatic degradation of AMP to adenosine could be ruled out, as AMP still elicited migration and changes in cytokine secretion in bone-marrow derived DCs generated from CD73-deficient animals and in human DCs pretreated with the ecto-nucleotidase inhibitor 5′-(alpha,beta-methylene) diphosphate (APCP). Finally, the influence of contaminating adenosine could be excluded, as AMP admixed with adenosine desaminase (ADA) was still able to influence DC function. In summary our data show that AMP when present during maturation is a potent regulator of dendritic cell function and point out the role for AMP in the pathogenesis of inflammatory disorders.
Role of cervical dendritic cell subsets, co-stimulatory molecules, cytokine secretion profile and beta-estradiol in development of sequalae to Chlamydia trachomatis infection
Tanvi Agrawal, Vikas Vats, Paul K Wallace, Sudha Salhan, Aruna Mittal
Reproductive Biology and Endocrinology , 2008, DOI: 10.1186/1477-7827-6-46
Abstract: Myeloid DCs (mDCs) and plasmacytoid DCs (pDCs) populations in cervical mucosa and peripheral blood were analyzed in controls and Chlamydia positive women with or without fertility disorders with multicoloured flow cytometric analysis. Cervical cytokines (IL-6, IL-8, IL-10, IL-12, TNF-alpha and IFN-gamma), C-reactive protein levels and sex hormone levels in serum were quantified by ELISA.In cervix of Chlamydia positive women with fertility disorders, significantly high (P < 0.05) numbers of pDCs were present with increased CD80 expression. pDCs correlated significantly with C-reactive protein levels, IL-6 and IFN-gamma levels in women with fertility disorders. In contrast, mDCs showed significant upregulation of CD1a during chlamydial infection and correlated significantly with IL-12 levels in Chlamydia positive fertile women. β-estradiol levels were significantly higher in women having fertility disorders as compared to fertile women and have significant correlations (r = 0.65; P < 0.05) with pDCs numbers, CD80 expression, IL-6 levels and IFN-gamma levels in these women.These results suggest that development of sequalae in some women can be a result of interplay of many factors including type of dendritic cell, co stimulatory molecule expression, cytokine secretion pattern and hormone levels.Chlamydia trachomatis infections are the most prevalent sexually transmitted bacterial infections worldwide [1]. In India, a high prevalence rate of genital chlamydial infection has been reported among symptomatic women, of which upto 30% have fertility related disorders as multiple spontaneous abortions, infertility (not male related), or sub fertility [2,3]. Spontaneous clearance of C. trachomatis from the lower genital tract occurs in nearly 20% of chlamydial infections without any sequelae [4], however, in absence of treatment, these infections often recur, or remain persistent, leading to structural damage to the inflamed tissue and increase the risk of developing a sequela
TLR7/TLR8 Activation Restores Defective Cytokine Secretion by Myeloid Dendritic Cells but Not by Plasmacytoid Dendritic Cells in HIV-Infected Pregnant Women and Newborns  [PDF]
Elaine Cristina Cardoso, Nátalli Zanete Pereira, Gabrielle Eimi Mitsunari, Luanda Mara da Silva Oliveira, Rosa Maria S. A. Ruocco, Rossana Pulcineli Vieira Francisco, Marcelo Zugaib, Alberto José da Silva Duarte, Maria Notomi Sato
PLOS ONE , 2013, DOI: 10.1371/journal.pone.0067036
Abstract: Mother-to-child transmission (MTCT) of HIV-1 has been significantly reduced with the use of antiretroviral therapies, resulting in an increased number of HIV-exposed uninfected infants. The consequences of HIV infection on the innate immune system of both mother-newborn are not well understood. In this study, we analyzed peripheral blood and umbilical cord blood (CB) collected from HIV-1-infected and uninfected pregnant women. We measured TNF-α, IL-10 and IFN-α secretion after the stimulation of the cells with agonists of both extracellular Toll-like receptors (TLRs) (TLR2, TLR4 and TLR5) and intracellular TLRs (TLR7, TLR7/8 and TLR9). Moreover, as an indicator of the innate immune response, we evaluated the responsiveness of myeloid dendritic cells (mDCs) and plasmacytoid DCs (pDCs) to TLRs that are associated with the antiviral response. Our results showed that peripheral blood mononuclear cells (PBMCs) from HIV-1-infected mothers and CB were defective in TNF-α production after activation by TLR2, TLR5, TLR3 and TLR7. However, the TNF-α response was preserved after TLR7/8 (CL097) stimulation, mainly in the neonatal cells. Furthermore, only CL097 activation was able to induce IL-10 and IFN-α secretion in both maternal and CB cells in the infected group. An increase in IFN-α secretion was observed in CL097-treated CB from HIV-infected mothers compared with control mothers. The effectiveness of CL097 stimulation was confirmed by observation of similar mRNA levels of interferon regulatory factor-7 (IRF-7), IFN-α and TNF-α in PBMCs of both groups. The function of both mDCs and pDCs was markedly compromised in the HIV-infected group, and although TLR7/TLR8 activation overcame the impairment in TNF-α secretion by mDCs, such stimulation was unable to reverse the dysfunctional type I IFN response by pDCs in the HIV-infected samples. Our findings highlight the dysfunction of innate immunity in HIV-infected mother-newborn pairs. The activation of the TLR7/8 pathway could function as an adjuvant to improve maternal-neonatal innate immunity.
Probiotic modulation of dendritic cells co-cultured with intestinal epithelial cells  [cached]
Ji Yeun Kim,Myeong Soo Park,Geun Eog Ji
World Journal of Gastroenterology , 2012, DOI: 10.3748/wjg.v18.i12.1308
Abstract: AIM: To investigate cytokine production and cell surface phenotypes of dendritic cells (DC) in the presence of epithelial cells stimulated by probiotics. METHODS: Mouse DC were cultured alone or together with mouse epithelial cell monolayers in normal or inverted systems and were stimulated with heat-killed probiotic bacteria, Bifidobacterium lactis AD011 (BL), Bifidobacterium bifidum BGN4 (BB), Lactobacillus casei IBS041 (LC), and Lactobacillus acidophilus AD031 (LA), for 12 h. Cytokine levels in the culture supernatants were determined by enzyme-linked immunosorbent assay and phenotypic analysis of DC was investigated by flow cytometry. RESULTS: BB and LC in single-cultured DC increased the expression of I-Ad, CD86 and CD40 (I-Ad, 18.51 vs 30.88, 46.11; CD86, 62.74 vs 92.7, 104.12; CD40, 0.67 vs 6.39, 3.37, P < 0.05). All of the experimental probiotics increased the production of inflammatory cytokines, interleukin (IL)-6 and tumor necrosis factor (TNF)-α. However, in the normal co-culture systems, LC and LA decreased the expression of I-Ad (39.46 vs 30.32, 33.26, P < 0.05), and none of the experimental probiotics increased the levels of IL-6 or TNF-α. In the inverted co-culture systems, LC decreased the expression of CD40 (1.36 vs -2.27, P < 0.05), and all of the experimental probiotics decreased the levels of IL-6. In addition, BL increased the production of IL-10 (103.8 vs 166.0, P < 0.05) and LC and LA increased transforming growth factor-β secretion (235.9 vs 618.9, 607.6, P < 0.05). CONCLUSION: These results suggest that specific probiotic strains exert differential immune modulation mediated by the interaction of dendritic cells and epithelial cells in the homeostasis of gastrointestinal tract.
Preparation of rat synovial membrane for studies of cytokine secretion.  [cached]
Anna Hyc,Anna Osiecka-Iwan,Piotr Dziunycz,Stanis?aw Moskalewski
Folia Histochemica et Cytobiologica , 2007, DOI: 10.5603/4553
Abstract: The objective of this work was to devise an in vitro system for studies on cytokine secretion by synovial membrane treated as a whole organ with various synoviocyte populations. Synovial membrane from knee joints of WAG rats was dissected and incubated in culture medium without serum for 4 - 48 h. The level of IL-1alpha was determined in synovial lysates and IL-6 in culture medium. The synovial membrane from left and right knee joint of the same rat produced similar amount of cytokines both in lysates and in the medium. Synovial membrane stimulated by LPS for 4 or 24 h gave significantly stronger cytokine response than the membrane from the opposite (control) knee. After 48 h incubation of synovial membrane drastic drop in cytokine level was noted, which indicated on deterioration of the membranes. The test may be useful in studies on factors affecting cytokine secretion by synoviocytes.
Human Intestinal Dendritic Cells Decrease Cytokine Release against Salmonella Infection in the Presence of Lactobacillus paracasei upon TLR Activation  [PDF]
Miriam Bermudez-Brito, Sergio Mu?oz-Quezada, Carolina Gomez-Llorente, Esther Matencio, María J. Bernal, Fernando Romero, Angel Gil
PLOS ONE , 2012, DOI: 10.1371/journal.pone.0043197
Abstract: Probiotic bacteria have been shown to modulate immune responses and could have therapeutic effects in allergic and inflammatory disorders. However, little is known about the signalling pathways that are engaged by probiotics. Dendritic cells (DCs) are antigen-presenting cells that are involved in immunity and tolerance. Monocyte-derived dendritic cells (MoDCs) and murine DCs are different from human gut DCs; therefore, in this study, we used human DCs generated from CD34+ progenitor cells (hematopoietic stem cells) harvested from umbilical cord blood; those DCs exhibited surface antigens of dendritic Langerhans cells, similar to the lamina propria DCs in the gut. We report that both a novel probiotic strain isolated from faeces of exclusively breast-fed newborn infants, Lactobacillus paracasei CNCM I-4034, and its cell-free culture supernatant (CFS) decreased pro-inflammatory cytokines and chemokines in human intestinal DCs challenged with Salmonella. Interestingly, the supernatant was as effective as the bacteria in reducing pro-inflammatory cytokine expression. In contrast, the bacterium was a potent inducer of TGF-β2 secretion, whereas the supernatant increased the secretion of TGF-β1 in response to Salmonella. We also showed that both the bacteria and its supernatant enhanced innate immunity through the activation of Toll-like receptor (TLR) signalling. These treatments strongly induced the transcription of the TLR9 gene. In addition, upregulation of the CASP8 and TOLLIP genes was observed. This work demonstrates that L. paracasei CNCM I-4034 enhanced innate immune responses, as evidenced by the activation of TLR signalling and the downregulation of a broad array of pro-inflammatory cytokines. The use of supernatants like the one described in this paper could be an effective and safe alternative to using live bacteria in functional foods.
Pycnogenol Augments Macrophage Phagocytosis and Cytokine Secretion  [PDF]
Vandana Shah,Erben Bayeta,Benjamin H.S. Lau
Pakistan Journal of Nutrition , 2002,
Abstract: We previously reported that Pycnogenol , procyanidins extracted from the bark of French maritime pine (Pinus maritima Aiton; the official botanical name is now Pinus pinaster Aiton) is a potent free radical scavenger. It has been shown to inhibit macrophage oxidative burst. Macrophages carry out their microbicidal and tumoricidal activities via oxygen-dependent and oxygen-independent mechanisms. The present study investigated the effects of Pycnogenol on oxygen-independent killing mechanisms of macrophages, with particular interest in phagocytosis and cytokine release. J774 cells, a murine macrophage cell line, were preincubated with Pycnogenol and then exposed to fluorescein-conjugated Escherichia coli particles for phagocytosis. Pycnogenol significantly enhanced the phagocytosis by J774 cells. Incubation with Pycnogenol resulted in a significant increase in cell size indicating macrophage activation. J774 cells were treated with Pycnogenol for 22 hr and the supernatants were tested for the release of tumor necrosis factor-α (TNF-α) and interleukin-1 β (IL-1β). Pycnogenol significantly increased the secretion of both TNF-α and IL-1β . These results suggest that Pycnogenol can enhance the macrophage function by increasing its ability to phagocytosis and secretion of TNF-α and IL-1β . These two cytokines may provide costimulatory signals to enhance both the humoral and cellular immune responses to promote host defense.
SHARPIN Is Essential for Cytokine Production, NF-κB Signaling, and Induction of Th1 Differentiation by Dendritic Cells  [PDF]
Zhe Wang, Anna Sokolovska, Rosemarie Seymour, John P. Sundberg, Harm HogenEsch
PLOS ONE , 2012, DOI: 10.1371/journal.pone.0031809
Abstract: Spontaneous mutations of the Sharpin (SHANK-associated RH domain-interacting protein, other aliases: Rbckl1, Sipl1) gene in mice result in systemic inflammation that is characterized by chronic proliferative dermatitis and dysregulated secretion of T helper1 (Th1) and Th2 cytokines. The cellular and molecular mechanisms underlying this inflammatory phenotype remain elusive. Dendritic cells may contribute to the initiation and progression of the phenotype of SHARPIN-deficient mice because of their pivotal role in innate and adaptive immunity. Here we show by flow cytometry that SHARPIN- deficiency did not alter the distribution of different DC subtypes in the spleen. In response to TOLL-like receptor (TLR) agonists LPS and poly I:C, cultured bone marrow-derived dendritic cells (BMDC) from WT and mutant mice exhibited similar increases in expression of co-stimulatory molecules CD40, CD80, and CD86. However, stimulated SHARPIN-deficient BMDC had reduced transcription and secretion of pro-inflammatory mediators IL6, IL12P70, GMCSF, and nitric oxide. Mutant BMDC had defective activation of NF-κB signaling, whereas the MAPK1/3 (ERK1/2) and MAPK11/12/13/14 (p38 MAP kinase isoforms) and TBK1 signaling pathways were intact. A mixed lymphocyte reaction showed that mutant BMDC only induced a weak Th1 immune response but stimulated increased Th2 cytokine production from allogeneic na?ve CD4+ T cells. In conclusion, loss of Sharpin in mice significantly affects the immune function of DC and this may partially account for the systemic inflammation and Th2-biased immune response.
Expression and cytokine secretion in the states of immune reactivation in leprosy
Sampaio, E.P.;Sarno, E.N.;
Brazilian Journal of Medical and Biological Research , 1998, DOI: 10.1590/S0100-879X1998000100009
Abstract: leprosy is a chronic inflammatory disease caused by mycobacterium leprae. the human response to this pathogen exhibits intriguing aspects which are up to now not well understood. the present study discusses the probable mechanisms involved in t cell-specific unresponsiveness observed in lepromatous patients. analysis of the cytokine profile either in blood leukocytes or in skin specimens taken from leprosy lesions indicates that some parameters of th1 immune response are present in lepromatous patients under reactional states
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