Whole virus influenza vaccine activates dendritic cells and promotes t helper-1 activity, while subunit vaccines stimulate T-cell proliferation

1998 ◽  
Vol 149 (1) ◽  
pp. 97 ◽  
Author(s):  
M. Saurwein-Teissl ◽  
K. Zisterer ◽  
T.L. Schmitt ◽  
R. Glück ◽  
S. Cryz ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Dendritic Cells ◽  
T Cell ◽  
Influenza Vaccine ◽  
T Cell Proliferation ◽  
T Helper ◽  
T Helper 1 ◽  
Subunit Vaccines ◽  
Virus Influenza

scholarly journals Evidence of Immunosuppressive and Th2 Immune Polarizing Effects of Antidiabetic Momordica charantia Fruit Juice

2017 ◽  
Vol 2017 ◽  
pp. 1-13 ◽  
Author(s):  
Rufine Fachinan ◽  
Adnette Fagninou ◽  
Magloire Pandoua Nekoua ◽  
Abdou Madjid Amoussa ◽  
Marius Adjagba ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
T Cell ◽  
Fruit Juice ◽  
Momordica Charantia ◽  
T Cell Proliferation ◽  
T Helper ◽  
T Helper 1 ◽  
T Helper 2 ◽  
Human T Cell ◽  
Cell Proliferation And Differentiation

The mechanism of action of the antidiabetic capacity of Momordica charantia is still under investigation. Here, we assessed phytochemical compositions, antioxidant activity, and effects of total and filtered fruit and leafy stem juices of Momordica charantia on human T cell proliferation and differentiation through quantification of Th1/Th2 cytokines. In the absence of stimulation, total fruit and leafy stem juices induced significant T cell proliferation. Under PHA stimulation, both juices potentiated plant-induced T cell proliferation. However, the filtered fruit and leafy stem juices significantly inhibited PHA-stimulated T cell proliferation, while neither juice influenced T cell proliferation. Moreover, total and filtered fruit juice increased IL-4 secretion, while total and filtered leafy stem juice enhanced IFN-γ production. Phytochemical screening revealed the presence of tannins, flavonoids, anthocyans, steroids, and triterpenoids in both juices. Alkaloids, quinone derivatives, cardenolides, and cyanogenic derivatives were undetectable. The saponins present in total juices were undetectable after filtration. Moreover, both juices had appreciable antioxidant capacity. Our study supports the type 1 antidiabetic effect of filtered fruit juice of M. charantia which may be related to its immunosuppressive and T-helper 2 cell inducing capacities. Due to their immune-stimulatory activities and their ability to increase T-helper 1 cell cytokines, total fruit and leafy stem juices may serve in the treatment of immunodeficiency and certain infections.

CD40-Licensing Of Human Dendritic Cells Further Matures Tnfa-Treated Dcs But Does Not Mediate Resistance Against Inhibition Of T-Cell Proliferation By TREG

Blood ◽  
2013 ◽  
Vol 122 (21) ◽  
pp. 4726-4726
Author(s):  
Matthias Eyrich ◽  
Johannes Rachor ◽  
Marissa Blume ◽  
Isabelle Becker ◽  
Anne Stumpf ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Dendritic Cells ◽  
T Cell ◽  
Cancer Immunotherapy ◽  
Cytokine Production ◽  
T Cell Proliferation ◽  
Autologous Tumor ◽  
T Helper ◽  
Cell Proliferation Inhibition ◽  
T Cell Priming

Vaccination with cytokine-matured dendritic cells (DCs), loaded with autologous tumor lysate, represents a promising strategy in cancer immunotherapy, however, in clinical trials vaccination with this kind of DCs has shown only limited efficacy so far. In animal experiments, CD40-licensing of DCs conveys resistance to tumor-induced immunosuppression including immunomodulation of regulatory T cells (Tregs). DCs were generated by differentiation of monocytes for 7 days with GM-CSF/IL-4 followed by 48h maturation with TFNα/IL-1ß ± CD40L. Then, DC were analyzed with respect to phenotype, cytokine production, and T-cell stimulatory capacity. CD40-licensed DCs showed higher expression of CD86 (MFI 3074±630 vs. 2433±359 with vs. without CD40L, respectively, p<.05) and a trend towards higher CD80, CD83 expression. Coculture of DCs with Tregs during maturation led to a reduction of costimulatory molecules, presumably by transendocytosis of Tregs. This phenomenon could be partially abrogated by CD40-licensing. TNFα/IL1ß-matured DCs produced significant amounts of IL-6, IL-8, TNFα, and IL-1ß. CD40-licensing did further increase cytokine production, however, no IL-12 could be detected. In contrast to murine DCs, a second round of LPS-stimulation after TNFα/IL1ß could not trigger IL-12 production. Control DCs matured with LPS/IFNγ showed up to 16% IL-12+ DCs. Using Melan-A as a model tumor antigen, priming capacity of CD40-licensed DCs to induce Melan-A specific CD8+ CTLs was slightly but not significantly improved compared to nonlicensed DCs, as demonstrated by somewhat higher frequencies of Melan-A multimer+ and TNFα+IFNγ+ CTLs after 11 days of culture with CD40-licensed DCs and rechallenge, respectively. Again, T-cell priming was best with control DCs matured with LPS/IFNγ. In contrast to T-cell priming, CD40-licensed DCs did not show any improved capacity to stimulate CD4+ T-helper cell proliferation. Furthermore, in a classcial MLR-suppression assay Tregs inhibited CD4+ T-helper proliferation by approx. 40%, this suppression was not alleviated by CD40-licensing of DCs. Interestingly, Treg proliferation in combined MLR-assays was increased in all experimental settings. Treg-suppression of CD4+ T-helper proliferation as well as the increased Treg-proliferation in the combined MLR-assays could not be prevented by the lysosomal inhibitor Bafilomycin A. This suggests, that other mechanisms than transendocytosis of costimulatory molcules by Tregs mediate these effects. In summary, these data show that CD40-licensing is a feasible tool to improve maturity of cytokine-treated DCs. However, CD40-licensing cannot induce IL-12 production in human DCs without TLR-stimulation and was not able to confer resistance against Treg-mediated T-cell proliferation inhibition. Thus, in order to strengthen DCs for cancer immunotherapy, CD40-licensing should be further investigated in combination with TLR-triggering DC-maturation cocktails. Disclosures: No relevant conflicts of interest to declare.

scholarly journals Myeloid Dendritic Cells from Human Cutaneous Squamous Cell Carcinoma Are Poor Stimulators of T-Cell Proliferation

2009 ◽  
Vol 129 (10) ◽  
pp. 2451-2462 ◽  
Author(s):  
Mark J. Bluth ◽  
Lisa C. Zaba ◽  
Dariush Moussai ◽  
Mayte Suárez-Fariñas ◽  
Helen Kaporis ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Squamous Cell Carcinoma ◽  
Dendritic Cells ◽  
T Cell ◽  
Cell Carcinoma ◽  
Squamous Cell ◽  
Cutaneous Squamous Cell Carcinoma ◽  
T Cell Proliferation ◽  
Myeloid Dendritic Cells

Flow cytometric analysis of T cell proliferation in a mixed lymphocyte reaction with dendritic cells

2003 ◽  
Vol 275 (1-2) ◽  
pp. 57-68 ◽  
Author(s):  
Xuan Duc Nguyen ◽  
Hermann Eichler ◽  
Alex Dugrillon ◽  
Christoph Piechaczek ◽  
Michael Braun ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Dendritic Cells ◽  
T Cell ◽  
Mixed Lymphocyte Reaction ◽  
Flow Cytometric Analysis ◽  
T Cell Proliferation ◽  
Flow Cytometric

Abstract 13287: Dendritic Cells Play a Critical Role in the Initiation of Atherosclerosis

Circulation ◽  
2014 ◽  
Vol 130 (suppl_2) ◽  
Author(s):  
Mengyao Jin ◽  
Peng Liu
Keyword(s):  
Cell Proliferation ◽  
Dendritic Cells ◽  
T Cell ◽  
T Cell Activation ◽  
Cell Activation ◽  
Critical Role ◽  
Cell Interaction ◽  
Plaque Formation ◽  
T Cell Proliferation ◽  
Control Group

Introduction: Dendritic cells (DCs) that are known as professional antigen-presenting cells have been found to pre-locate in non-inflammatory arterial wall and increasingly accumulate during atherosclerosis progression. Previous findings suggested that residential DCs in the intima are responsible for capturing modified lipids and forming foam cells during the initiation of atherosclerosis. Hypothesis: DC accumulation and enhanced DC-T cell interaction play a critical role in the initiation of atherosclerosis. Methods: We measured plaque formation, vascular DC accumulation and antigen-specific T cell proliferation mediated by isolated aortic cells in ApoE-/- mice, as well as DTR-CD11c/ApoE-/- or DTR-CD11b/ApoE-/- mice for conditional depletion of DCs or macrophages, respectively. A brief high-fat diet for 10 days was used as a model of initial atherosclerosis. Results: In addition to increased intimal DC accumulation and plaque formation in aortic roots, 10 days of HFD induced T cell infiltration in ApoE-/- mice, compared to those without HFD as the control. Isolated aortic cells from mice with 10-day HFD showed stronger capability in inducing antigen-specific T cell proliferation, compare to the control (HFD: 3.14±0.71%; no HFD: 1.56±0.36%; p=0.022). Single diphtheria toxin (DT) injection at day 1 yielded approximately 50% decrease in intimal DC accumulation, as well as 60% attenuation in plaque formation in DTR-CD11c/ApoE-/- mice after 10-day HFD. Capability of stimulating antigen-specific T cell proliferation was also impaired in aortic cells from DC-depleted mice (DT-treated: 1.62±0.30%; PBS-treated: 3.04±0.59%; p= 0.004), along with reduction in indirect conduction of T cell activation. In contrast, no significant changes were found in plaque formation and DC accumulation in DT-injected DTR-CD11b/ApoE-/- mice after 10 days of HFD, compared to control group. Furthermore, depletion of CD11b+ macrophages in either aortas or spleens didn’t alter capability of inducing antigen-specific T cell proliferation in DT-injected mice. Conclusions: These results suggested that vascular DCs rather than macrophages play a more important role in T cell activation and initiation of atherosclerosis.

scholarly journals HIV inhibits CD4+ T-cell proliferation by inducing indoleamine 2,3-dioxygenase in plasmacytoid dendritic cells

Blood ◽  
2006 ◽  
Vol 109 (8) ◽  
pp. 3351-3359 ◽  
Author(s):  
Adriano Boasso ◽  
Jean-Philippe Herbeuval ◽  
Andrew W. Hardy ◽  
Stephanie A. Anderson ◽  
Matthew J. Dolan ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Dendritic Cells ◽  
T Cell ◽  
Functional Impairment ◽  
Plasmacytoid Dendritic Cells ◽  
Cd4 T Cell ◽  
T Cell Proliferation ◽  
Type I ◽  
Indoleamine 2,3 Dioxygenase

AbstractInfection with the human immunodeficiency virus type-1 (HIV) results in acute and progressive numeric loss of CD4+ T-helper cells and functional impairment of T-cell responses. The mechanistic basis of the functional impairment of the surviving cells is not clear. Indoleamine 2,3-dioxygenase (IDO) is an immunosuppressive enzyme that inhibits T-cell proliferation by catabolizing the essential amino acid tryptophan (Trp) into the kynurenine (kyn) pathway. Here, we show that IDO mRNA expression is elevated in peripheral blood mononuclear cells (PBMCs) from HIV+ patients compared with uninfected healthy controls (HCs), and that in vitro inhibition of IDO with the competitive blocker 1-methyl tryptophan (1-mT) results in increased CD4+ T-cell proliferative response in PBMCs from HIV-infected patients. We developed an in vitro model in which exposure of PBMCs from HCs to either infectious or noninfectious, R5- or X4-tropic HIV induced IDO in plasmacytoid dendritic cells (pDCs). HIV-induced IDO was not inhibited by blocking antibodies against interferon type I or type II, which, however, induced IDO in pDCs when added to PBMC cultures. Blockade of gp120/CD4 interactions with anti-CD4 Ab inhibited HIV-mediated IDO induction. Thus, induction of IDO in pDCs by HIV may contribute to the T-cell functional impairment observed in HIV/AIDS by a non–interferon-dependent mechanism.

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