scholarly journals Role of beta1 and beta2 subunits of the interleukin-12 receptor in determining T helper 1/T helper 2 responses in vivo in the rat

Immunology ◽  
2000 ◽  
Vol 99 (1) ◽  
pp. 109-112 ◽  
Author(s):  
K. M. Gillespie ◽  
C.-C. Szeto ◽  
V. M. Betin ◽  
P. W. Mathieson
Keyword(s):  
Interleukin 12 ◽  
T Helper ◽  
T Helper 1 ◽  
T Helper 2

scholarly journals The Th1:Th2 Dichotomy of Pregnancy and Preterm Labour

2012 ◽  
Vol 2012 ◽  
pp. 1-12 ◽  
Author(s):  
Lynne Sykes ◽  
David A. MacIntyre ◽  
Xiao J. Yap ◽  
Tiong Ghee Teoh ◽  
Phillip R. Bennett
Keyword(s):  
Pregnancy Loss ◽  
Preterm Labour ◽  
Adverse Outcomes ◽  
T Helper ◽  
T Helper 1 ◽  
T Helper 2 ◽  
Infection And Inflammation ◽  
Therapeutic Measures ◽  
New Biomarkers

Pregnancy is a unique immunological state in which a balance of immune tolerance and suppression is needed to protect the fetus without compromising the mother. It has long been established that a bias from the T helper 1 cytokine profile towards the T helper 2 profile contributes towards successful pregnancy maintenance. The majority of publications that report on aberrant Th1:Th2 balance focus on early pregnancy loss and preeclampsia. Over the last few decades, there has been an increased awareness of the role of infection and inflammation in preterm labour, and the search for new biomarkers to predict preterm labour continues. In this paper, we explore the evidence for an aberrant Th1:Th2 profile associated with preterm labour. We also consider the potential for its use in screening women at high risk of preterm labour and for prophylactic therapeutic measures for the prevention of preterm labour and associated neonatal adverse outcomes.

scholarly journals Limited role of CD28-mediated signals in T helper subset differentiation.

1996 ◽  
Vol 184 (3) ◽  
pp. 803-810 ◽  
Author(s):  
D R Brown ◽  
J M Green ◽  
N H Moskowitz ◽  
M Davis ◽  
C B Thompson ◽  
...  
Keyword(s):  
T Cell Differentiation ◽  
Interleukin 4 ◽  
T Helper ◽  
T Helper 1 ◽  
Absolute Requirement ◽  
Costimulatory Signals ◽  
Draining Lymph Nodes

The role of CD28-mediated signals in T helper cell maturation is not fully understood. We tested the requirement for costimulation through CD28 in several systems of CD4+, T cell differentiation. In vivo priming of mice with genetic disruption of CD28 (CD28-/-) yielded normal levels of antigen-specific interferon gamma production but markedly diminished levels of interleukin 4 (IL-4) after in vitro restimulation. In response to the pathogenic microbe, Leishman a major, C57BL6 CD28-/- mice were fully capable of controlling infection and exhibited a normal T helper 1 response. BALB/c CD28-/- mice unexpectedly exhibited normal susceptibility to L. major. BALB/c CD28-/- mice developed high levels of IL-4 mRNA and protein induction in the draining lymph nodes. In addition, susceptibility of BALB/c CD28-/- mice was reversed by neutralization of IL-4 in vivo. We also activated transgenic CD28-bearing T cells from the BALB and C57BL background in vitro in the presence of CTLA4Ig. BALB cells had greater IL-4 producing capacity than C57BL cells in the absence of costimulation. Diverse factors including costimulatory signals, genetic polymorphism, and the nature of the immunogen all influence T helper phenotype commitment, but these results provide evidence that CD28 is not an absolute requirement for generating either Th1 or Th2 responses.

scholarly journals P-Selectin Glycoprotein Ligand 1 (Psgl-1) Is a Physiological Ligand for E-Selectin in Mediating T Helper 1 Lymphocyte Migration

2000 ◽  
Vol 192 (11) ◽  
pp. 1669-1676 ◽  
Author(s):  
Takako Hirata ◽  
Glenn Merrill-Skoloff ◽  
Melissa Aab ◽  
Jing Yang ◽  
Barbara C. Furie ◽  
...  
Keyword(s):  
Contact Hypersensitivity ◽  
Th1 Cells ◽  
Wild Type ◽  
T Helper ◽  
Lymphocyte Migration ◽  
T Helper 1 ◽  
Deficient Mice

P-selectin glycoprotein ligand 1 (PSGL-1) is a sialomucin expressed on leukocytes that mediates neutrophil rolling on the vascular endothelium. Here, the role of PSGL-1 in mediating lymphocyte migration was studied using mice lacking PSGL-1. In a contact hypersensitivity model, the infiltration of CD4+ T lymphocytes into the inflamed skin was reduced in PSGL-1–deficient mice. In vitro–generated T helper (Th)1 cells from PSGL-1–deficient mice did not bind to P-selectin and migrated less efficiently into the inflamed skin than wild-type Th1 cells. To assess the role of PSGL-1 in P- or E-selectin–mediated migration of Th1 cells, the cells were injected into E- or P-selectin–deficient mice. PSGL-1–deficient Th1 cells did not migrate into the inflamed skin of E-selectin–deficient mice, indicating that PSGL-1 on Th1 cells is the sole ligand for P-selectin in vivo. In contrast, PSGL-1–deficient Th1 cells migrated into the inflamed skin of P-selectin–deficient mice, although less efficiently than wild-type Th1 cells. This E-selectin–mediated migration of PSGL-1–deficient or wild-type Th1 cells was not altered by injecting a blocking antibody to L-selectin. These data provide evidence that PSGL-1 on Th1 cells functions as one of the E-selectin ligands in vivo.

scholarly journals The Selenoprotein MsrB1 Instructs Dendritic Cells to Induce T-Helper 1 Immune Responses

Antioxidants ◽  
2020 ◽  
Vol 9 (10) ◽  
pp. 1021
Author(s):  
Ho-Jae Lee ◽  
Joon Seok Park ◽  
Hyun Jung Yoo ◽  
Hae Min Lee ◽  
Byung Cheon Lee ◽  
...  
Keyword(s):  
Dendritic Cells ◽  
T Cell ◽  
Immune Responses ◽  
Therapeutic Potential ◽  
Methionine Sulfoxide Reductase ◽  
Interleukin 12 ◽  
T Helper ◽  
T Helper 1

Immune activation associates with the intracellular generation of reactive oxygen species (ROS). To elicit effective immune responses, ROS levels must be balanced. Emerging evidence shows that ROS-mediated signal transduction can be regulated by selenoproteins such as methionine sulfoxide reductase B1 (MsrB1). However, how the selenoprotein shapes immunity remains poorly understood. Here, we demonstrated that MsrB1 plays a crucial role in the ability of dendritic cells (DCs) to provide the antigen presentation and costimulation that are needed for cluster of differentiation antigen four (CD4) T-cell priming in mice. We found that MsrB1 regulated signal transducer and activator of transcription-6 (STAT6) phosphorylation in DCs. Moreover, both in vitro and in vivo, MsrB1 potentiated the lipopolysaccharide (LPS)-induced Interleukin-12 (IL-12) production by DCs and drove T-helper 1 (Th1) differentiation after immunization. We propose that MsrB1 activates the STAT6 pathway in DCs, thereby inducing the DC maturation and IL-12 production that promotes Th1 differentiation. Additionally, we showed that MsrB1 promoted follicular helper T-cell (Tfh) differentiation when mice were immunized with sheep red blood cells. This study unveils as yet unappreciated roles of the MsrB1 selenoprotein in the innate control of adaptive immunity. Targeting MsrB1 may have therapeutic potential in terms of controlling immune reactions.

scholarly journals Interleukin-18 plays a role in both the alum-induced T helper 2 response and the T helper 1 response induced by alum-adsorbed interleukin-12

Immunology ◽  
2003 ◽  
Vol 108 (2) ◽  
pp. 137-143 ◽  
Author(s):  
Kevin G. J. Pollock ◽  
Margaret Conacher ◽  
Xiao-Qing Wei ◽  
James Alexander ◽  
James M. Brewer
Keyword(s):  
Interleukin 12 ◽  
Interleukin 18 ◽  
T Helper ◽  
T Helper 1 ◽  
T Helper 2

scholarly journals Biophysical Attributes of CpG Presentation Control TLR9 Signaling to Differentially Polarize Systemic Immune-Responses

2016 ◽  
Author(s):  
Jardin A. Leleux ◽  
Pallab Pradhan ◽  
Krishnendu Roy
Keyword(s):  
Dc Programming ◽  
T Helper ◽  
T Helper 1 ◽  
T Helper 2 ◽  
Stat3 Phosphorylation ◽  
Pathogen Recognition Receptors ◽  
Sense And Respond ◽  
Tlr9 Signaling ◽  
Biophysical Attributes

AbstractIt is currently unknown whether and how mammalian pathogen-recognition receptors (PRR) respond to biophysical patterns of pathogen-associated molecular danger-signals. Using synthetic pathogen-like particles (PLPs) that mimic physical properties of bacteria or large-viruses, we have discovered that the quality and quantity of Toll-like-receptor-9 (TLR9)-signaling by CpG in mouse dendritic cells (mDC) is uniquely dependent on biophysical attributes, specifically the surface-density of CpG and size of the presenting PLP. These physical patterns control DC-programming by regulating kinetics and magnitude of MyD88-IRAK4 signaling, NFκB-driven responses, and STAT3 phosphorylation, which in turn controls differential T cell responses and in vivo immune-polarization, especially T-helper 1 (Th1) versus T-helper 2 (Th2) antibody responses. Our findings suggest that innate immune cells can sense and respond not only to molecular, but also pathogen-associated physical patterns (PAPPs), broadening the tools for modulating immunity, helping to better understand innate response mechanisms to pathogens and develop new and improved vaccines.

scholarly journals Vernal keratoconjunctivitis in human immunodeficiency virus – The possible role of T-helper 1–T-helper 2 shift

2018 ◽  
Vol 66 (7) ◽  
pp. 1004 ◽  
Author(s):  
Bhaskar Srinivasan ◽  
Shweta Agarwal ◽  
Geetha Iyer ◽  
Sridharan Sudharshan ◽  
Kavita Kalaivani
Keyword(s):  
Human Immunodeficiency Virus ◽  
Vernal Keratoconjunctivitis ◽  
T Helper ◽  
T Helper 1 ◽  
T Helper 2 ◽  
Immunodeficiency Virus

scholarly journals High Levels of Susceptibility and T Helper 2 Response in MyD88-Deficient Mice Infected with Leishmania major Are Interleukin-4 Dependent

2003 ◽  
Vol 71 (12) ◽  
pp. 7215-7218 ◽  
Author(s):  
Andrea Debus ◽  
Joachim Gläsner ◽  
Martin Röllinghoff ◽  
André Gessner
Keyword(s):  
Knockout Mice ◽  
Leishmania Major ◽  
Parasite Burden ◽  
Interleukin 4 ◽  
Myeloid Differentiation ◽  
Interleukin 12 ◽  
T Helper ◽  
T Helper 1 ◽  
T Helper 2 ◽  
Deficient Mice

ABSTRACT Myeloid differentiation protein 88 (MyD88) is a general adaptor for the signaling cascade through receptors of the Toll/IL-1R family. When infected with Leishmania major parasites, MyD88-deficient mice displayed a dramatically enhanced parasite burden in their tissues similar to that found in susceptible BALB/c mice. In contrast, MyD88 knockout mice did not develop ulcerating lesions despite a lack of interleukin-12 (IL-12) production and a predominant T helper 2 cell response. Blockade of IL-4 produced early (day 1) after infection restored a protective T helper 1 response in MyD88 knockout mice.

scholarly journals P-Selectin Glycoprotein Ligand-1 (PSGL-1) on T Helper 1 but Not on T Helper 2 Cells Binds to P-Selectin and Supports Migration into Inflamed Skin

1997 ◽  
Vol 185 (3) ◽  
pp. 573-578 ◽  
Author(s):  
Eric Borges ◽  
Wolfgang Tietz ◽  
Martin Steegmaier ◽  
Thomas Moll ◽  
Rupert Hallmann ◽  
...  
Keyword(s):  
Delayed Type Hypersensitivity ◽  
Th2 Cells ◽  
Th1 Cells ◽  
T Helper ◽  
T Helper 1 ◽  
T Helper 2 ◽  
Affinity Isolation ◽  
Blocking Activity ◽  
Selectin Binding

We have shown recently that mouse Th1 cells but not Th2 cells are selectively recruited into inflamed sites of a delayed-type hypersensitivity (DTH) reaction of the skin. This migration was blocked by monoclonal antibodies (mAb) against P- and E-selectin. Here we show that Th1 cells bind to P-selectin via the P-selectin glycoprotein ligand-1 (PSGL-1). This is the only glycoprotein ligand that was detectable by affinity isolation with a P-selectin–Ig fusion protein. Binding of Th1 cells to P-selectin, as analyzed by flow cytometry and in cell adhesion assays, was completely blocked by antibodies against PSGL-1. The same antibodies blocked partially the migration of Th1 cells into cutaneous DTH reactions. This blocking activity, in combination with that of a mAb against E-selectin, was additive. PSGL-1 on Th2 cells, although expressed at similar levels as on Th1 cells, did not support binding to P-selectin. Thus, the P-selectin–binding form of PSGL-1 distinguishes Th1 cells from Th2 cells. Furthermore, PSGL-1 is relevant for the entry of Th1 cells into inflamed areas of the skin. This is the first demonstration for the importance of PSGL-1 for mouse leukocyte recruitment in vivo.

Sign in / Sign up

Export Citation Format

Share Document