Heat-Killed Cells of Lactobacilli Skew the Immune Response Toward T Helper 1 Polarization in Mouse Splenocytes and Dendritic Cell-Treated T Cells

2007 ◽  
Vol 55 (26) ◽  
pp. 11080-11086 ◽  
Author(s):  
Lisa Chuang ◽  
Keh-Gong Wu ◽  
Cindy Pai ◽  
Pei-Shan Hsieh ◽  
Jaw-Ji Tsai ◽  
...  
Keyword(s):  
Immune Response ◽  
T Cells ◽  
Dendritic Cell ◽  
T Helper ◽  
T Helper 1 ◽  
Mouse Splenocytes

scholarly journals The Role of Dendritic Cells in TB and HIV Infection

2020 ◽  
Vol 9 (8) ◽  
pp. 2661
Author(s):  
Rachel Abrahem ◽  
Emerald Chiang ◽  
Joseph Haquang ◽  
Amy Nham ◽  
Yu-Sam Ting ◽  
...  
Keyword(s):  
Immune Response ◽  
T Cells ◽  
Dendritic Cells ◽  
Dendritic Cell ◽  
Hiv Infection ◽  
Cell Response ◽  
Defense Mechanism ◽  
Critical Role ◽  
Cytokine Release ◽  
T Helper 1

Dendritic cells are the principal antigen-presenting cells (APCs) in the host defense mechanism. An altered dendritic cell response increases the risk of susceptibility of infections, such as Mycobacterium tuberculosis (M. tb), and the survival of the human immunodeficiency virus (HIV). The altered response of dendritic cells leads to decreased activity of T-helper-1 (Th1), Th2, Regulatory T cells (Tregs), and Th17 cells in tuberculosis (TB) infections due to a diminishment of cytokine release from these APCs, while HIV infection leads to DC maturation, allowing DCs to migrate to lymph nodes and the sub-mucosa where they then transfer HIV to CD4 T cells, although there is controversy around this topic. Increases in the levels of the antioxidant glutathione (GSH) plays a critical role in maintaining dendritic cell redox homeostasis, leading to an adequate immune response with sufficient cytokine release and a subsequent robust immune response. Thus, an understanding of the intricate pathways involved in the dendritic cell response are needed to prevent co-infections and co-morbidities in individuals with TB and HIV.

scholarly journals Can levamisole upregulate the equine cell‐mediated macrophage (M1) dendritic cell (DC1) T‐helper 1 (CD4 Th1) T‐cytotoxic (CD8) immune response in vitro?

2019 ◽  
Vol 33 (2) ◽  
pp. 889-896 ◽  
Author(s):  
Sharon Witonsky ◽  
Virginia Buechner‐Maxwell ◽  
Amy Santonastasto ◽  
Robert Pleasant ◽  
Stephen Werre ◽  
...  
Keyword(s):  
Immune Response ◽  
Dendritic Cell ◽  
T Helper ◽  
T Helper 1 ◽  
Immune Response In Vitro

scholarly journals Mycobacterium tuberculosisProtein Rv3841 Activates Dendritic Cells and Contributes to a T Helper 1 Immune Response

2018 ◽  
Vol 2018 ◽  
pp. 1-13 ◽  
Author(s):  
Seunga Choi ◽  
Han-Gyu Choi ◽  
Ki-Won Shin ◽  
Yong Woo Back ◽  
Hye-Soo Park ◽  
...  
Keyword(s):  
Immune Response ◽  
T Cells ◽  
Dendritic Cells ◽  
Protective Efficacy ◽  
Mitogen Activated Protein Kinase ◽  
T Helper ◽  
T Helper 1 ◽  
Cell Immunity ◽  
Mitogen Activated Protein ◽  
Mycobacterial Growth

The attenuated vaccineMycobacterium bovisBCG (Bacille Calmette Guerin) has limited protective efficacy against TB. The development of more effective TB vaccines has focused on the mycobacterial antigens that cause strong T helper 1 (Th1) responses. Mtb protein Rv3841 (bacterioferritin B; BfrB) is known to play a crucial role in the growth of Mtb. Nonetheless, it is unclear whether Rv3841 can induce protective immunity against Mtb. Here, we studied the action of Rv3841 in maturation of dendritic cells (DCs) and its engagement in the development of T-cell immunity. We found that Rv3841 functionally activated DCs by upregulating costimulatory molecules and increased secretion of proinflammatory cytokines. Activation of DCs by Rv3841 was mediated by Toll-like receptor 4 (TLR4), followed by triggering of mitogen-activated protein kinase and nuclear factor-κB signaling pathways. In addition, Rv3841-matured DCs effectively proliferated and polarized Th1 immune response of naïve CD4+and CD8+T-cells. Moreover, Rv3841 specifically caused the expansion of CD4+CD44highCD62LlowT-cells from Mtb-infected mice; besides, the T-cells activated by Rv3841-matured DCs inhibited intracellular mycobacterial growth. Our data suggest that Rv3841 induces DC maturation and protective immune responses, a finding that may provide candidate of effective TB vaccines.

scholarly journals Arginine Enhances Induction of T Helper 1 and T Helper 2 Cytokine Synthesis by Peyer’s Patch αβ T Cells and Antigen-Specific Mucosal Immune Response

1998 ◽  
Vol 62 (12) ◽  
pp. 2334-2340 ◽  
Author(s):  
Toshiya KOBAYASHI ◽  
Masafumi YAMAMOTO ◽  
Takachika HIROI ◽  
Jerry MCGHEE ◽  
Yasuyoshi TAKESHITA ◽  
...  
Keyword(s):  
Immune Response ◽  
T Cells ◽  
Mucosal Immune Response ◽  
Peyer’S Patch ◽  
T Helper ◽  
Peyer's Patch ◽  
T Helper 1 ◽  
T Helper 2 ◽  
Cytokine Synthesis ◽  
Αβ T Cells

scholarly journals Midazolam Suppresses Maturation of Murine Dendritic Cells and Priming of Lipopolysaccharide-induced T Helper 1-type Immune Response

2011 ◽  
Vol 114 (2) ◽  
pp. 355-362 ◽  
Author(s):  
Noriyuki Ohta ◽  
Yoshifumi Ohashi ◽  
Chihiro Takayama ◽  
Takashi Mashimo ◽  
Yuji Fujino
Keyword(s):  
Immune Response ◽  
T Cells ◽  
Benzodiazepine Receptor ◽  
Contact Hypersensitivity ◽  
Interleukin 12 ◽  
Peripheral Benzodiazepine Receptor ◽  
T Helper ◽  
T Helper 1 ◽  
Mixed Cell ◽  
Histocompatibility Complex

Background Dendritic cells (DCs), as antigen-presenting cells, play a key role in the induction and regulation of adaptive immune response. Midazolam is reported to have immunomodulatory properties that affect immune cells. However, the effect of midazolam on DCs has not been characterized. We examined the immunomodulatory properties of midazolam on DC-mediated immune response. Methods After allowing murine bone marrow-derived DCs induced by granulocyte macrophage colony stimulating factor to mature, we analyzed their expression of costimulatory molecules (CD80 and CD86), major histocompatibility complex class II molecules, and the secretion of interleukin-12 p40. In vitro, we evaluated the effect of midazolam on maturing DCs in mixed cell cultures containing DCs and T cells. In vivo, we investigated the contact-hypersensitivity response. Results Midazolam suppressed the expression of CD80, CD86, and major histocompatibility complex class II molecules from murine DCs. Treated with midazolam, DCs also secreted less interleukin-12 p40. In mixed cell cultures with CD3-positive T cells, midazolam-treated DCs showed less propensity to stimulate the proliferation of CD3-positive T cells and the secretion of interferon-γ from CD4-positive T cells. Midazolam-treated DCs impaired the induction of contact-hypersensitivity response. Treatment with ligands for peripheral benzodiazepine receptor inhibited the up-regulation of CD80 during DC maturation. Conclusion Midazolam inhibits the functional maturation of murine DCs and interferes with DC induction of T helper 1 immunity in the whole mouse. In addition, it appears that the immunomodulatory effect of midazolam is mediated via the action of midazolam on the peripheral benzodiazepine receptor.

Haloperidol Suppresses Murine Dendritic Cell Maturation and Priming of the T Helper 1–Type Immune Response

2015 ◽  
Vol 120 (4) ◽  
pp. 895-902 ◽  
Author(s):  
Atsuhiro Matsumoto ◽  
Noriyuki Ohta ◽  
Yukiko Goto ◽  
Yozo Kashiwa ◽  
Shunsuke Yamamoto ◽  
...  
Keyword(s):  
Immune Response ◽  
Dendritic Cell ◽  
Dendritic Cell Maturation ◽  
Cell Maturation ◽  
T Helper ◽  
T Helper 1

scholarly journals OX40L–OX40 Signaling in Atopic Dermatitis

2021 ◽  
Vol 10 (12) ◽  
pp. 2578
Author(s):  
Masutaka Furue ◽  
Mihoko Furue
Keyword(s):  
T Cells ◽  
Atopic Dermatitis ◽  
Memory T Cells ◽  
Effector Memory ◽  
T Helper ◽  
T Helper 1 ◽  
Therapeutic Success ◽  
T Helper 2 ◽  
Promising Target ◽  
Antigen Presenting

OX40 is one of the co-stimulatory molecules expressed on T cells, and it is engaged by OX40L, primarily expressed on professional antigen-presenting cells such as dendritic cells. The OX40L–OX40 axis is involved in the sustained activation and expansion of effector T and effector memory T cells, but it is not active in naïve and resting memory T cells. Ligation of OX40 by OX40L accelerates both T helper 1 (Th1) and T helper 2 (Th2) effector cell differentiation. Recent therapeutic success in clinical trials highlights the importance of the OX40L–OX40 axis as a promising target for the treatment of atopic dermatitis.

scholarly journals Development of Autologous, Oligoclonal, Poorly Functioning T Lymphocytes in a Patient With Autosomal Recessive Severe Combined Immunodeficiency Caused by Defects of the Jak3 Tyrosine Kinase

Blood ◽  
1998 ◽  
Vol 91 (3) ◽  
pp. 949-955 ◽  
Author(s):  
Duilio Brugnoni ◽  
Luigi D. Notarangelo ◽  
Alessandra Sottini ◽  
Paolo Airò ◽  
Marta Pennacchio ◽  
...  
Keyword(s):  
T Cells ◽  
T Lymphocytes ◽  
Tyrosine Kinase ◽  
Cd4 T Cells ◽  
Severe Combined Immunodeficiency ◽  
Combined Immunodeficiency ◽  
T Helper ◽  
T Helper 1 ◽  
In Vitro Susceptibility ◽  
And Function

Abstract Defects of the common gamma chain subunit of the cytokine receptors (γc) or of Jak3, a tyrosine kinase required for γc signal transduction, result in T−B+ severe combined immunodeficiency (SCID). However, atypical cases, characterized by progressive development of T lymphocytes, have been also reported. We describe a child with SCID caused by Jak3 gene defects, which strongly but not completely affect Jak3 protein expression and function, who developed a substantial number (>3,000/μL) of autologous CD3+CD4+ T cells. These cells showed a primed/activated phenotype (CD45R0+ Fas+HLA-DR+ CD62Llo), defective secretion of T-helper 1 and T-helper 2 cytokines, reduced proliferation to mitogens, and a high in vitro susceptibility to spontaneous (caused by downregulation of bcl-2 expression) as well as activation-induced cell death. A restricted T-cell receptor repertoire was observed, with oligoclonal expansion within each of the dominant segments. These features resemble those observed in γc-/y and in Jak3−/−mice, in which a population of activated, anergic T cells (predominantly CD4+) also develops with age. These results suggest that residual Jak3 expression and function or other Jak3-independent signals may also permit the generation of CD4+ T cells that undergo in vivo clonal expansion in humans; however, these mechanisms do not allow development of CD8+ T cells, nor do they fully restore the functional properties of CD4+ T lymphocytes.

676 FINE SPECIFICITY OF ANTI-NUP62 T-HELPER 1 CELL (TH1) IMMUNE RESPONSE IN PRIMARY BILIARY CIRRHOSIS

2009 ◽  
Vol 50 ◽  
pp. S248 ◽  
Author(s):  
F. Meda ◽  
M.S. Longhi ◽  
D.P. Bogdanos ◽  
P. Invernizzi ◽  
Y. Ma ◽  
...  
Keyword(s):  
Immune Response ◽  
Primary Biliary Cirrhosis ◽  
Biliary Cirrhosis ◽  
T Helper ◽  
T Helper 1 ◽  
Fine Specificity ◽  
Th1 Immune Response

scholarly journals T helper cell polarisation as a measure of the maturation of the immune response

2003 ◽  
Vol 12 (5) ◽  
pp. 285-292 ◽  
Author(s):  
Scott B. Cameron ◽  
Ellen H. Stolte ◽  
Anthony W. Chow ◽  
Huub F. J. Savelkoul
Keyword(s):  
Immune Response ◽  
T Cells ◽  
Intracellular Cytokine Staining ◽  
T Helper Cell ◽  
Helper Cell ◽  
Enzyme Linked Immunosorbent Assay ◽  
Intracellular Cytokine ◽  
T Helper

Background:T helper cell polarisation is important under chronic immune stimulatory conditions and drives the type of the evolving immune response. Mice treated with superantigensin vivodisplay strong effects on Thsubset differentiation. The aim of the study was to detect the intrinsic capacity of T cells to polarise under variousex vivoconditions.Methods:Purified CD4+T cells obtained from superantigen-treated mice were cultured under Thpolarising conditionsin vitro. By combining intracellular cytokine staining and subsequent flow cytometric analysis with quantitative cytokine measurements in culture supernatants by enzyme-linked immunosorbent assay (ELISA), the differential Thpolarising capacity of the treatment can be detected in a qualitative and quantitative manner.Results and conclusions:BALB/c mice were shown to be biased to develop strong Th2 polarised immune responses using Th0 stimulation of purified CD4+T cells from phosphate-buffered saline-treated mice. Nevertheless, our analysis methodology convincingly showed that even in these mice, Toxic Shock Syndrome Toxin-1 treatmentin vivoresulted in a significantly stronger Th1 polarising effect than control treatment. Our results indicate that populations of Thcells can be assessed individually for their differential Th1 or Th2 maturation capacityin vivoby analysing robustin vitropolarisation cultures combined with intracellular cytokine staining and ELISA.

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