scholarly journals Estradiol enhances primary antigen-specific CD4 T cell responses and Th1 development in vivo. Essential role of estrogen receptor α expression in hematopoietic cells

2003 ◽  
Vol 33 (2) ◽  
pp. 512-521 ◽  
Author(s):  
Arlette Maret ◽  
Jérôme D. Coudert ◽  
Lucile Garidou ◽  
Gilles Foucras ◽  
Pierre Gourdy ◽  
...  
Keyword(s):  
Estrogen Receptor ◽  
T Cell ◽  
Essential Role ◽  
Hematopoietic Cells ◽  
T Cell Responses ◽  
Estrogen Receptor Α ◽  
Cd4 T Cell ◽  
Cell Responses

scholarly journals Role of B cells as antigen-presenting cells in vivo revisited: antigen-specific B cells are essential for T cell expansion in lymph nodes and for systemic T cell responses to low antigen concentrations

2001 ◽  
Vol 13 (12) ◽  
pp. 1583-1593 ◽  
Author(s):  
Amariliz Rivera ◽  
Chiann-Chyi Chen ◽  
Naomi Ron ◽  
Joseph P. Dougherty ◽  
Yacov Ron
Keyword(s):  
T Cell ◽  
B Cells ◽  
Lymph Nodes ◽  
Cell Expansion ◽  
T Cell Responses ◽  
Antigen Presenting Cells ◽  
Cell Responses ◽  
Antigen Presenting

scholarly journals Assessment of CD4+ T Cell Responses to Glutamic Acid Decarboxylase 65 Using DQ8 Tetramers Reveals a Pathogenic Role of GAD65 121–140 and GAD65 250–266 in T1D Development

PLoS ONE ◽  
2014 ◽  
Vol 9 (11) ◽  
pp. e112882 ◽  
Author(s):  
I-Ting Chow ◽  
Junbao Yang ◽  
Theresa J. Gates ◽  
Eddie A. James ◽  
Duy T. Mai ◽  
...  
Keyword(s):  
T Cell ◽  
Glutamic Acid ◽  
Glutamic Acid Decarboxylase ◽  
T Cell Responses ◽  
Cd4 T Cell ◽  
Acid Decarboxylase ◽  
Pathogenic Role ◽  
Cell Responses ◽  
Glutamic Acid Decarboxylase 65

scholarly journals TRANCE, a Tumor Necrosis Factor Family Member Critical for CD40 Ligand–independent T Helper Cell Activation

1999 ◽  
Vol 189 (7) ◽  
pp. 1025-1031 ◽  
Author(s):  
Martin F. Bachmann ◽  
Brian R. Wong ◽  
Régis Josien ◽  
Ralph M. Steinman ◽  
Annette Oxenius ◽  
...  
Keyword(s):  
T Cell ◽  
Family Member ◽  
T Cell Responses ◽  
Cd40 Ligand ◽  
Cd4 T Cell ◽  
Cell Responses ◽  
T Cell Priming ◽  
Deficient Mice ◽  
Necrosis Factor

CD40 ligand (CD40L), a tumor necrosis factor (TNF) family member, plays a critical role in antigen-specific T cell responses in vivo. CD40L expressed on activated CD4+ T cells stimulates antigen-presenting cells such as dendritic cells, resulting in the upregulation of costimulatory molecules and the production of various inflammatory cytokines required for CD4+ T cell priming in vivo. However, CD40L- or CD40-deficient mice challenged with viruses mount protective CD4+ T cell responses that produce normal levels of interferon γ, suggesting a CD40L/CD40-independent mechanism of CD4+ T cell priming that to date has not been elucidated. Here we show that CD4+ T cell responses to viral infection were greatly diminished in CD40-deficient mice by administration of a soluble form of TNF-related activation-induced cytokine receptor (TRANCE-R) to inhibit the function of another TNF family member, TRANCE. Thus, the TRANCE/TRANCE-R interaction provides costimulation required for efficient CD4+ T cell priming during viral infection in the absence of CD40L/CD40. These results also indicate that not even the potent inflammatory microenvironment induced by viral infections is sufficient to elicit efficient CD4+ T cell priming without proper costimulation provided by the TNF family (CD40L or TRANCE). Moreover, the data suggest that TRANCE/TRANCE-R may be a novel and important target for immune intervention.

CpG oligonucleotides induce strong humoral but only weak CD4+ T cell responses to protein antigens in rhesus macaques in vivo

Vaccine ◽  
2005 ◽  
Vol 23 (25) ◽  
pp. 3310-3317 ◽  
Author(s):  
Gunther Hartmann ◽  
Anja Marschner ◽  
Pablo Renner Viveros ◽  
Christiane Stahl-Hennig ◽  
Martin Eisenblätter ◽  
...  
Keyword(s):  
T Cell ◽  
Rhesus Macaques ◽  
T Cell Responses ◽  
Cd4 T Cell ◽  
Protein Antigens ◽  
Cell Responses ◽  
Cpg Oligonucleotides

The role of CD4+ T cell responses in antitumor immunity

1998 ◽  
Vol 10 (5) ◽  
pp. 588-594 ◽  
Author(s):  
Drew M Pardoll ◽  
Suzanne L Topalian
Keyword(s):  
T Cell ◽  
Antitumor Immunity ◽  
T Cell Responses ◽  
Cd4 T Cell ◽  
Cell Responses

scholarly journals In Vivo Suppression of Naive CD4 T Cell Responses by IL-2- and Antigen-Stimulated T Lymphocytes in the Absence of APC Competition

2008 ◽  
Vol 181 (5) ◽  
pp. 3323-3335 ◽  
Author(s):  
Hiroto Inaba ◽  
Meredith Steeves ◽  
Phuong Nguyen ◽  
Terrence L. Geiger
Keyword(s):  
T Cell ◽  
T Lymphocytes ◽  
T Cell Responses ◽  
Cd4 T Cell ◽  
Cell Responses

scholarly journals Studying the immunosuppressive role of indoleamine 2,3-dioxygenase: tryptophan metabolites suppress rat allogeneic T-cell responses in vitro and in vivo

2005 ◽  
Vol 18 (1) ◽  
pp. 95-100 ◽  
Author(s):  
Thomas M. Bauer ◽  
Lucian P. Jiga ◽  
Jing-Jing Chuang ◽  
Marco Randazzo ◽  
Gerhard Opelz ◽  
...  
Keyword(s):  
T Cell ◽  
T Cell Responses ◽  
Cell Responses ◽  
Indoleamine 2,3 Dioxygenase ◽  
Tryptophan Metabolites

scholarly journals Sting Negatively Regulates Allogeneic T-Cell Responses By Constraining Antigen-Presenting Cell Function

Blood ◽  
2020 ◽  
Vol 136 (Supplement 1) ◽  
pp. 37-38
Author(s):  
Yongxia Wu ◽  
Chih-Hang Anthony Tang ◽  
Corey Mealer ◽  
David Bastian ◽  
Mohammed Hanief Sofi ◽  
...  
Keyword(s):  
T Cells ◽  
T Cell ◽  
Conflicts Of Interest ◽  
Hematopoietic Cells ◽  
T Cell Responses ◽  
Receptor Expression ◽  
Constitutive Activation ◽  
Cell Responses ◽  
And Function

The endoplasmic-reticulum-resident protein STING (Stimulator of IFN genes) is a downstream signaling effector of cytosolic DNA sensor cGAS (cyclic GMP-AMP synthase). STING-mediated innate immune activation plays a key role in tumor- and self-DNA elicited anti-tumor immunity and autoimmunity, respectively, yet the mechanism remains largely unclear. We utilized murine models of allogeneic hematopoietic cell transplantation (allo-HCT) to study the biology of STING in antigen-presetting cells (APCs) and T cells. STING expression in donor T cells was dispensable for their ability to induce graft-versus-host disease (GVHD), a major complication of allo-HCT in the clinic. However, when STING-deficient mice were used as recipients, more severe disease was induced after allo-HCT. Using bone marrow (BM) chimeras where STING was absent in different compartments, we found that STING-deficiency on host hematopoietic cells (Fig. A), but not on non-hematopoietic cells, was primarily responsible for exacerbating the disease. Furthermore, STING expression on host CD11c+ cells played a dominant role in the regulation of allogeneic T-cell responses (Fig. B). Mechanistically, STING deficiency resulted in increased survival, activation and function of irradiated APCs, including macrophages and dendritic cells (DCs, fig. C-D). To further determine the role of STING in APCs, we generated a STING V154M knock-in mouse model, in which V154M mutation in TMEM173 causes constitutive activation of STING. Consistently, constitutive activation of STING attenuated the survival, activation and function of APCs isolated from STING V154M knock-in mice. In addition, STING-deficient APCs augmented donor T-cell expansion, chemokine receptor expression and migration into intestinal tissues (Fig. E), resulting in accelerated/exacerbated disease. Using pharmacologic approaches, we demonstrate that systemic administration of a STING agonist (c-di-GMP) to recipient mice before transplantation significantly reduced GVHD mortality (Fig. F). In conclusion, we report an inhibitory role of STING in regulating survival and T-cell priming function of hematopoietic APCs, especially CD11c+ cells, after allo-HCT. We validate that pharmacological activation of STING may serve as a potential therapeutic strategy to constrain APCs and induce immune tolerance. Figure Disclosures No relevant conflicts of interest to declare.

Sign in / Sign up

Export Citation Format

Share Document