scholarly journals Efficient Induction of CCR9 on T Cells Requires Coactivation of Retinoic Acid Receptors and Retinoid X Receptors (RXRs): Exaggerated T Cell Homing to the Intestine by RXR Activation with Organotins

2010 ◽  
Vol 185 (9) ◽  
pp. 5289-5299 ◽  
Author(s):  
Hajime Takeuchi ◽  
Aya Yokota ◽  
Yoshiharu Ohoka ◽  
Hiroyuki Kagechika ◽  
Chieko Kato ◽  
...  
1992 ◽  
Vol 89 (6) ◽  
pp. 2321-2325 ◽  
Author(s):  
B. Blumberg ◽  
D. J. Mangelsdorf ◽  
J. A. Dyck ◽  
D. A. Bittner ◽  
R. M. Evans ◽  
...  

mBio ◽  
2020 ◽  
Vol 11 (2) ◽  
Author(s):  
Jennifer D. Helble ◽  
Rodrigo J. Gonzalez ◽  
Ulrich H. von Andrian ◽  
Michael N. Starnbach

ABSTRACT While there is no effective vaccine against Chlamydia trachomatis infection, previous work has demonstrated the importance of C. trachomatis-specific CD4+ T cells (NR1 T cells) in pathogen clearance. Specifically, NR1 T cells have been shown to be protective in mice, and this protection depends on the host’s ability to sense the cytokine gamma interferon (IFN-γ). However, it is unclear what role NR1 production or sensing of IFN-γ plays in T cell homing to the genital tract or T cell-mediated protection against C. trachomatis. Using two-photon microscopy and flow cytometry, we found that naive wild-type (WT), IFN-γ−/−, and IFN-γR−/− NR1 T cells specifically home to sections in the genital tract that contain C. trachomatis. We also determined that protection against infection requires production of IFN-γ from either NR1 T cells or endogenous cells, further highlighting the importance of IFN-γ in clearing C. trachomatis infection. IMPORTANCE Chlamydia trachomatis is an important mucosal pathogen that is the leading cause of sexually transmitted bacterial infections in the United States. Despite this, there is no vaccine currently available. In order to develop such a vaccine, it is necessary to understand the components of the immune response that can lead to protection against this pathogen. It is well known that antigen-specific CD4+ T cells are critical for Chlamydia clearance, but the contexts in which they are protective or not protective are unknown. Here, we aimed to characterize the importance of gamma interferon production and sensing by T cells and the effects on the immune response to C. trachomatis. Our work here helps to define the contexts in which antigen-specific T cells can be protective, which is critical to our ability to design an effective and protective vaccine against C. trachomatis.


1999 ◽  
Vol 19 (4) ◽  
pp. 338-347 ◽  
Author(s):  
Jacques J.M. Janssen ◽  
Eleonoor D. Kuhlmann ◽  
Anke H.M. van Vugt ◽  
Huub J. Winkens ◽  
Bert P.M. Janssen ◽  
...  

Autoimmunity ◽  
1992 ◽  
Vol 13 (2) ◽  
pp. 117-126 ◽  
Author(s):  
Tomas Olsson ◽  
Per Diener ◽  
Åke Ljungdahl ◽  
Bo Höjeberg ◽  
Peter H. Van Der Meide ◽  
...  

Development ◽  
1997 ◽  
Vol 124 (2) ◽  
pp. 515-523 ◽  
Author(s):  
C.R. Sharpe ◽  
K. Goldstone

Retinoid receptors, which are members of the nuclear hormone receptor superfamily, act as ligand-dependent transcription factors. They mediate the effects of retinoic acid primarily as heterodimers of retinoic acid receptors (RARs) and retinoid X receptors (RXRs). To analyse their function, xRXR beta synthetic mRNA was injected into Xenopus embryos in combination with normal and mutated xRAR alpha transcripts. Two informative phenotypes are reported here. Firstly, over-expression of xRXR beta with xRAR alpha results in the formation of ectopic primary neurons. Secondly, blocking retinoid signalling with a mutated xRAR alpha results in a lack of primary neurons. These two phenotypes, from contra-acting manipulations, indicate a role for retinoid signalling during neurogenesis.


1992 ◽  
Vol 12 (11) ◽  
pp. 4862-4871
Author(s):  
B J Aneskievich ◽  
E Fuchs

Terminal differentiation of epidermal keratinocytes is inhibited by 1 microM retinoic acid, a concentration which induces differentiation in a number of cell types, including F9 teratocarcinoma cells. The molecular basis for these opposing retinoid responses is unknown, although retinoic acid receptors (RARs) and retinoid X receptors (RXRs) have been detected in both cell types. When F9 cells are stably transfected with a truncated RAR alpha lacking the E/F domain necessary for ligand binding and RAR/RXR dimerization, action at retinoid response elements is suppressed and cells produce a retinoic acid-resistant phenotype; i.e., they are blocked in differentiation (A. S. Espeseth, S. P. Murphy, and E. Linney, Genes Dev. 3:1647-1656, 1989). If retinoid receptors influence epidermal differentiation only in a negative fashion, then suppression of transactivation at retinoid response elements would be expected to enhance, rather than block, keratinocyte differentiation. In this study, we show that surprisingly, even though constitutive expression of an analogous truncated RAR gamma in keratinocytes specifically suppressed transactivation at retinoid response elements, keratinocytes were blocked, rather than enhanced, in their ability to undergo morphological and biochemical features of differentiation. These findings demonstrate a direct and hitherto unrecognized role for RARs and RXRs in positively as well as negatively regulating epidermal differentiation. Additionally, our studies extend those of Espeseth et al. (Genes Dev. 3:1647-1656, 1989), indicating a novel RAR function independent of the E/F domain.


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