scholarly journals C-Reactive Protein Directly Suppresses Th1 Cell Differentiation and Alleviates Experimental Autoimmune Encephalomyelitis

2015 ◽  
Vol 194 (11) ◽  
pp. 5243-5252 ◽  
Author(s):  
Lin Zhang ◽  
Shan-Hui Liu ◽  
Tyler T. Wright ◽  
Zhi-Yuan Shen ◽  
Hai-Yun Li ◽  
...  
Keyword(s):  
Cell Differentiation ◽  
Experimental Autoimmune Encephalomyelitis ◽  
C Reactive Protein ◽  
Autoimmune Encephalomyelitis ◽  
Th1 Cell ◽  
Reactive Protein ◽  
Experimental Autoimmune

scholarly journals Inhibition of Experimental Autoimmune Encephalomyelitis in Human C-Reactive Protein Transgenic Mice Is FcRIIB Dependent

2011 ◽  
Vol 2011 ◽  
pp. 1-6 ◽  
Author(s):  
Xian-Zhen Hu ◽  
Tyler T. Wright ◽  
Nicholas R. Jones ◽  
Theresa N. Ramos ◽  
Gregory A. Skibinski ◽  
...  
Keyword(s):  
Experimental Autoimmune Encephalomyelitis ◽  
Transgenic Mice ◽  
Fc Receptors ◽  
Subcutaneous Administration ◽  
Wild Type ◽  
C Reactive Protein ◽  
Autoimmune Encephalomyelitis ◽  
Similar Treatment ◽  
Reactive Protein ◽  
Experimental Autoimmune

We showed earlier that experimental autoimmune encephalomyelitis (EAE) in human C-reactive protein (CRP) transgenic mice (CRPtg) has delayed onset and reduced severity compared to wild-type mice. Since human CRP is known to engage Fc receptors and Fc receptors are known to play a role in EAE in the mouse, we sought to determine if FcRI, FcRIIb, or FcRIII was needed to manifest human CRP-mediated protection of CRPtg. We report here that in CRPtg lacking either of the two activating receptors, FcRI and FcRIII, the beneficial effects of human CRP are still observed. In contrast, if CRPtg lack expression of the inhibitory receptor FcRIIB, then the beneficial effect of human CRP is abrogated. Also, subcutaneous administration of purified human CRP stalled progression of ongoing EAE in wild-type mice, but similar treatment failed to impede EAE progression in mice lacking FcRIIB. The results reveal that a axis is responsible for protection against EAE in the CRPtg model.

scholarly journals Hepatic but Not CNS-Expressed Human C-Reactive Protein Inhibits Experimental Autoimmune Encephalomyelitis in Transgenic Mice

2015 ◽  
Vol 2015 ◽  
pp. 1-8 ◽  
Author(s):  
Tyler T Wright ◽  
Rachel V. Jimenez ◽  
Todd E. Morgan ◽  
Namrata Bali ◽  
Xiaogang Hou ◽  
...  
Keyword(s):  
Experimental Autoimmune Encephalomyelitis ◽  
Transgenic Mice ◽  
Gene Promoter ◽  
C Reactive Protein ◽  
Autoimmune Encephalomyelitis ◽  
Reactive Protein ◽  
Protective Actions ◽  
Dependent Protein ◽  
Low Levels ◽  
Experimental Autoimmune

We recently demonstrated that human C-reactive protein (CRP), expressed hepatically in transgenic mice (CRPtg), improved the outcome of experimental autoimmune encephalomyelitis (EAE), a murine model of multiple sclerosis (MS). The liver is the primary site of CRP synthesis in humans and in CRPtg mice but is also expressed by both at low levels in the CNS. To determine if CNS expression of human CRP is sufficient to impact EAE, we generated neuronal CRP transgenic mice (nCRPtg) wherein human CRP expression is driven by the neuron-specific Ca2+/calmodulin-dependent protein kinase IIα(CaMKIIα) gene promoter. We found that hepatically expressed/blood-borne CRP, but not CNS expressed CRP, lessened EAE severity. These outcomes indicate that the protective actions of human CRP in EAE are manifested in the periphery and not in the CNS and reveal a previously unappreciated site specificity for the beneficial actions of CRP in CNS disease.

scholarly journals The CTRP3-AdipoR2 Axis Regulates the Development of Experimental Autoimmune Encephalomyelitis by Suppressing Th17 Cell Differentiation

2021 ◽  
Vol 12 ◽  
Author(s):  
Masanori A. Murayama ◽  
Hsi-Hua Chi ◽  
Mako Matsuoka ◽  
Takahiro Ono ◽  
Yoichiro Iwakura
Keyword(s):  
T Cells ◽  
Cell Differentiation ◽  
Experimental Autoimmune Encephalomyelitis ◽  
Th17 Cell ◽  
Autoimmune Encephalomyelitis ◽  
Th1 Cell ◽  
Th17 Cell Differentiation ◽  
Good Target ◽  
Complement C1q ◽  
Experimental Autoimmune

C1q/TNF-related proteins (CTRP) including CTRP3 are a group of secreted proteins which have a complement C1q-like domain in common, and play versatile roles in lipid metabolism, inflammation, tumor metastasis and bone metabolism. Previously, we showed that the expression of C1qtnf3, encoding CTRP3, is highly augmented in joints of autoimmune arthritis models and CTRP3-deficiency exacerbates collagen-induced arthritis in mice. However, the mechanisms how CTRP3-deficiency exacerbates arthritis still remain to be elucidated. In this study, we showed that CTRP3 was highly expressed in Th17 cell, a key player for the development of autoimmune diseases, and Th17 cell differentiation was augmented in C1qtnf3–/– mice. Th17 cell differentiation, but not Th1 cell differentiation, was suppressed by CTRP3 and this suppression was abolished by the treatment with a receptor antagonist against AdipoR2, but not AdipoR1, associated with suppression of Rorc and Stat3 expression. Furthermore, AdipoR1 and AdipoR2 agonist, AdipoRon suppressed Th17 cell differentiation via AdipoR2, but not AdipoR1. The development of myelin oligodendrocyte glycoprotein (MOG)-induced experimental autoimmune encephalomyelitis was enhanced in C1qtnf3–/– mice associated with increase of Th17 cell population. CTRP3 inhibited MOG-induced IL-17 production from T cells by affecting both T cells and dendritic cells. These results show that CTRP3 is an endogenous regulator of Th17 differentiation, suggesting that the CTRP3-AdipoR2 axis is a good target for the treatment of Th17 cell-mediated diseases.

scholarly journals RGC-32 promotes Th17 cell differentiation and enhances experimental autoimmune encephalomyelitis

Immunobiology ◽  
2016 ◽  
Vol 221 (10) ◽  
pp. 1173
Author(s):  
Violeta Rus ◽  
Vinh Nguyen ◽  
Alexandru Tatomir ◽  
Dallas Boodhoo ◽  
Armugam P. Mekala ◽  
...  
Keyword(s):  
Cell Differentiation ◽  
Experimental Autoimmune Encephalomyelitis ◽  
Th17 Cell ◽  
Autoimmune Encephalomyelitis ◽  
Th17 Cell Differentiation ◽  
Experimental Autoimmune

scholarly journals RGC-32 Promotes Th17 Cell Differentiation and Enhances Experimental Autoimmune Encephalomyelitis

2017 ◽  
Vol 198 (10) ◽  
pp. 3869-3877 ◽  
Author(s):  
Violeta Rus ◽  
Vinh Nguyen ◽  
Alexandru Tatomir ◽  
Jason R. Lees ◽  
Armugam P. Mekala ◽  
...  
Keyword(s):  
Cell Differentiation ◽  
Experimental Autoimmune Encephalomyelitis ◽  
Th17 Cell ◽  
Autoimmune Encephalomyelitis ◽  
Th17 Cell Differentiation ◽  
Experimental Autoimmune
Sign in / Sign up

Export Citation Format

Share Document