scholarly journals Cockroach Allergen Bla g 7 Promotes TIM4 Expression in Dendritic Cells Leading to Th2 Polarization

2013 ◽  
Vol 2013 ◽  
pp. 1-10 ◽  
Author(s):  
Lingxiao Xu ◽  
Miaojia Zhang ◽  
Wenjing Ma ◽  
Shanshan Jin ◽  
Weijuan Song ◽  
...  
Keyword(s):  
T Cells ◽  
Dendritic Cells ◽  
Cd4 T Cells ◽  
Allergic Diseases ◽  
Cockroach Allergen ◽  
Th2 Polarization ◽  
Indoor Aeroallergens ◽  
Cockroach Allergy

As one of the most common sources of indoor aeroallergens worldwide, cockroach is important in causing rhinitis and asthma while the mechanisms underlying remain obscure. Since T helper (Th) type 2 polarization plays an important role in the pathogenesis of allergic diseases, we investigated the effect of Bla g 7, a pan-allergen fromBlattella germanica(B. germanica), on Th polarization which is controlled by monocyte-derived dendritic cells (DCs). Challenged by recombinant Bla g 7 (rBla g 7), immature DCs obtained from human exhibited upregulated levels of TIM4, CD80, and CD86 and increased IL-13 secretion. Cocultured with CD4+ T cells, challenged DCs increased the ratio of IL-4+ versus IFN-γ+ of CD4+ T cells, suggesting a balance shift from Th1 to Th2. Moreover, antibodies against TIM4, CD80, and CD86 reversed the enhancement of IL-4+/IFN-γ+ ratio and alleviated the IL-13 release induced by rBla g 7, indicating that the Th2 polarization provoked by rBla g 7 challenged DCs is via TIM4-, CD80-, and CD86-dependent mechanisms. In conclusion, the present findings implied a crucial role of Bla g 7 in the development of cockroach allergy and highlighted an involvement of DCs-induced Th2 polarization in cockroach allergy.

scholarly journals Role of dendritic cells infected with human herpesvirus 6 in virus transmission to CD4+ T cells

Virology ◽  
2009 ◽  
Vol 385 (2) ◽  
pp. 294-302 ◽  
Author(s):  
Masaya Takemoto ◽  
Takayoshi Imasawa ◽  
Koichi Yamanishi ◽  
Yasuko Mori
Keyword(s):  
T Cells ◽  
Dendritic Cells ◽  
Cd4 T Cells ◽  
Virus Transmission ◽  
Human Herpesvirus ◽  
Human Herpesvirus 6 ◽  
Herpesvirus 6

scholarly journals Innate Immune Responses to Herpes Simplex Virus Type 2 Influence Skin Homing Molecule Expression by Memory CD4+ Lymphocytes

2006 ◽  
Vol 80 (6) ◽  
pp. 2863-2872 ◽  
Author(s):  
David M. Koelle ◽  
Jay Huang ◽  
Michael T. Hensel ◽  
Christopher L. McClurkan
Keyword(s):  
T Cells ◽  
Dendritic Cells ◽  
Herpes Simplex Virus ◽  
Herpes Simplex ◽  
Cd4 T Cells ◽  
Receptor Expression ◽  
Homing Receptor ◽  
Skin Homing ◽  
Simplex Virus

ABSTRACT Herpes simplex virus (HSV) infections of humans are characterized by intermittent, lytic replication in epithelia. Circulating HSV-specific CD4 T cells express lower levels of preformed cutaneous lymphocyte-associated antigen (CLA), a skin-homing receptor, than do circulating HSV-specific CD8 T cells but, paradoxically, move into infected skin earlier than CD8 cells. Memory CD4 T cells develop strong and selective expression of CLA and E-selectin ligand while responding to HSV antigen in vitro. We now show that interleukin-12, type I interferon, and transforming growth factor beta are each involved in CLA expression by memory HSV type 2 (HSV-2)-specific CD4 T cells in peripheral blood mononuclear cells (PBMC). A reduction of the number of monocytes and dendritic cells from PBMC reduces CLA expression by HSV-2-responsive CD4 lymphoblasts, while their reintroduction restores this phenotype, identifying these cells as possible sources of CLA-promoting cytokines. Plasmacytoid dendritic cells are particularly potent inducers of CLA on HSV-reactive CD4 T cells. These observations are consistent with cooperation between innate and acquired immunity to promote a pattern of homing receptor expression that is physiologically appropriate for trafficking to infected tissues.

scholarly journals DC-SIGN–mediated Infectious Synapse Formation Enhances X4 HIV-1 Transmission from Dendritic Cells to T Cells

2004 ◽  
Vol 200 (10) ◽  
pp. 1279-1288 ◽  
Author(s):  
Jean-François Arrighi ◽  
Marjorie Pion ◽  
Eduardo Garcia ◽  
Jean-Michel Escola ◽  
Yvette van Kooyk ◽  
...  
Keyword(s):  
T Cells ◽  
Dendritic Cells ◽  
T Cell ◽  
Hiv Infection ◽  
Cd4 T Cells ◽  
Synapse Formation ◽  
Model Systems ◽  
Hiv 1 ◽  
Infectious Synapse

Dendritic cells (DCs) are essential for the early events of human immunodeficiency virus (HIV) infection. Model systems of HIV sexual transmission have shown that DCs expressing the DC-specific C-type lectin DC-SIGN capture and internalize HIV at mucosal surfaces and efficiently transfer HIV to CD4+ T cells in lymph nodes, where viral replication occurs. Upon DC–T cell clustering, internalized HIV accumulates on the DC side at the contact zone (infectious synapse), between DCs and T cells, whereas HIV receptors and coreceptors are enriched on the T cell side. Viral concentration at the infectious synapse may explain, at least in part, why DC transmission of HIV to T cells is so efficient. Here, we have investigated the role of DC-SIGN on primary DCs in X4 HIV-1 capture and transmission using small interfering RNA–expressing lentiviral vectors to specifically knockdown DC-SIGN. We demonstrate that DC-SIGN− DCs internalize X4 HIV-1 as well as DC-SIGN+ DCs, although binding of virions is reduced. Strikingly, DC-SIGN knockdown in DCs selectively impairs infectious synapse formation between DCs and resting CD4+ T cells, but does not prevent the formation of DC–T cells conjugates. Our results demonstrate that DC-SIGN is required downstream from viral capture for the formation of the infectious synapse between DCs and T cells. These findings provide a novel explanation for the role of DC-SIGN in the transfer and enhancement of HIV infection from DCs to T cells, a crucial step for HIV transmission and pathogenesis.

scholarly journals Correction: Human CD141+ Dendritic Cells Induce CD4+ T Cells To Produce Type 2 Cytokines

2014 ◽  
Vol 193 (12) ◽  
pp. 6210-6210 ◽  
Author(s):  
Chun I. Yu ◽  
Christian Becker ◽  
Patrick Metang ◽  
Florentina Marches ◽  
Yuanyuan Wang ◽  
...  
Keyword(s):  
T Cells ◽  
Dendritic Cells ◽  
Cd4 T Cells ◽  
Type 2 Cytokines

scholarly journals Independent Prognostic Potential of GNPNAT1 in Lung Adenocarcinoma

2020 ◽  
Vol 2020 ◽  
pp. 1-16
Author(s):  
Xiangyu Zheng ◽  
Yongwei Li ◽  
Chao Ma ◽  
Jinjun Zhang ◽  
Yanmin Zhang ◽  
...  
Keyword(s):  
T Cells ◽  
Dendritic Cells ◽  
B Cells ◽  
Lung Adenocarcinoma ◽  
Cd4 T Cells ◽  
Prognostic Value ◽  
Marker Genes ◽  
Immune Signatures ◽  
Cox Analysis

Background. Glucosamine-Phosphate N-Acetyltransferase 1 (GNPNAT1) is a critical enzyme in the biosynthesis of uridine diphosphate-N-acetylglucosamine. It has many important functions, such as protein binding, monosaccharide binding, and embryonic development and growth. However, the role of GNPNAT1 in lung adenocarcinoma (LUAD) remains unclear. Methods. In this study, we explored the expression pattern and prognostic value of GNPNAT1 in LUAD across TCGA and GEO databases and assessed its independent prognostic value via Cox analysis. LinkedOmics and GEPIA2 were applied to investigate coexpression and functional networks associated with GNPNAT1. The TIMER web tool was deployed to assess the correlation between GNPNAT1 and the main six types of tumor-infiltrating immune cells. Besides, the correlations between GNPNAT1 and the LUAD common genetic mutations, TMB, and immune signatures were examined. Results. GNPNAT1 was validated upregulated in tumor tissues in TCGA-LUAD and GEO cohorts. Moreover, in both TCGA and GEO cohorts, high GNPNAT1 expression was found to be associated with poor overall survival. Cox analysis showed that high GNPNAT1 expression was an independent risk factor for LUAD. Functional network analysis suggested that GNPNAT1 regulates cell cycle, ribosome, proteasome, RNA transport, and spliceosome signaling through pathways involving multiple cancer-related kinases and E2F family. In addition, GNPNAT1 correlated with infiltrating levels of B cells, CD4+ T cells, and dendritic cells. B cells and dendritic cells could predict the outcome of LUAD, and B cells and CD4+ T cells were significant independent risk factors. The TMB and mutations of KRAS, EGFR, STK11, and TP53 were correlated with GNPNAT1. At last, the correlation analysis showed GNPNAT1 correlated with most of the immune signatures we performed. Conclusion. Our findings showed that GNPNAT1 was correlated to the prognosis and immune infiltration of LUAD. In particular, the tight relationship between GNPNAT1 and B cell marker genes may be the epicenter of the immune response and one of the key factors affecting the prognosis. Our findings laid the foundation for further research on the immunomodulatory role of GNPNAT1 in LUAD.

scholarly journals Essential Role of Lung Plasmacytoid Dendritic Cells in Preventing Asthmatic Reactions to Harmless Inhaled Antigen

2004 ◽  
Vol 200 (1) ◽  
pp. 89-98 ◽  
Author(s):  
Hendrik Jan de Heer ◽  
Hamida Hammad ◽  
Thomas Soullié ◽  
Daniëlle Hijdra ◽  
Nanda Vos ◽  
...  
Keyword(s):  
T Cells ◽  
Dendritic Cells ◽  
Inflammatory Responses ◽  
Immunoglobulin E ◽  
Atopic Asthma ◽  
Cell Hyperplasia ◽  
Asthma Model ◽  
Th2 Cell

Tolerance is the usual outcome of inhalation of harmless antigen, yet T helper (Th) type 2 cell sensitization to inhaled allergens induced by dendritic cells (DCs) is common in atopic asthma. Here, we show that both myeloid (m) and plasmacytoid (p) DCs take up inhaled antigen in the lung and present it in an immunogenic or tolerogenic form to draining node T cells. Strikingly, depletion of pDCs during inhalation of normally inert antigen led to immunoglobulin E sensitization, airway eosinophilia, goblet cell hyperplasia, and Th2 cell cytokine production, cardinal features of asthma. Furthermore, adoptive transfer of pDCs before sensitization prevented disease in a mouse asthma model. On a functional level, pDCs did not induce T cell division but suppressed the generation of effector T cells induced by mDCs. These studies show that pDCs provide intrinsic protection against inflammatory responses to harmless antigen. Therapies exploiting pDC function might be clinically effective in preventing the development of asthma.

scholarly journals NIK signaling in dendritic cells but not in T cells is required for the development of effector T cells and cell-mediated immune responses

2011 ◽  
Vol 208 (9) ◽  
pp. 1917-1929 ◽  
Author(s):  
Janin Hofmann ◽  
Florian Mair ◽  
Melanie Greter ◽  
Marc Schmidt-Supprian ◽  
Burkhard Becher
Keyword(s):  
T Cells ◽  
Dendritic Cells ◽  
Immune Responses ◽  
Cd4 T Cells ◽  
Driving Force ◽  
Th17 Cells ◽  
Effector T Cells ◽  
Cell Mediated Immunity ◽  
Systematic Analysis

The canonical NF-κB pathway is a driving force for virtually all aspects of inflammation. Conversely, the role of the noncanonical NF-κB pathway and its central mediator NF-κB–inducing kinase (NIK) remains poorly defined. NIK has been proposed to be involved in the formation of TH17 cells, and its absence in TH cells renders them incapable of inducing autoimmune responses, suggesting a T cell–intrinsic role for NIK. Upon systematic analysis of NIK function in cell-mediated immunity, we found that NIK signaling is dispensable within CD4+ T cells but played a pivotal role in dendritic cells (DCs). We discovered that NIK signaling is required in DCs to deliver co-stimulatory signals to CD4+ T cells and that DC-restricted expression of NIK is sufficient to restore TH1 and TH17 responses as well as cell-mediated immunity in NIK−/− mice. When CD4+ T cells developed in the absence of NIK-sufficient DCs, they were rendered anergic. Reintroduction of NIK into DCs allowed developing NIK−/− CD4+ T cells to become functional effector populations and restored the development of autoimmune disease. Therefore, our data suggest that a population of thymic DCs requires NIK to shape the formation of most αβ CD4+ T effector lineages during early development.

Contribution of CD4+T Cells and Dendritic Cells to Female-Dominant Antigen-Induced T Helper Type 2 Cytokine Production by Bronchial Lymph Node Cells

2013 ◽  
Vol 161 (s2) ◽  
pp. 58-65 ◽  
Author(s):  
Kaori Okuyama ◽  
Masatoshi Suenaga ◽  
Shyunya Furuki ◽  
Tasuku Kawano ◽  
Yuichi Ohkawara ◽  
...  
Keyword(s):  
T Cells ◽  
Dendritic Cells ◽  
Lymph Node ◽  
Cd4 T Cells ◽  
Cytokine Production ◽  
T Helper ◽  
Lymph Node Cells ◽  
Bronchial Lymph Node ◽  
Helper Type
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