Inconsistence between number and function of autoreactive T cells in the course of experimental autoimmune encephalomyelitis

2017 ◽  
Vol 47 (1) ◽  
pp. 1-17 ◽  
Author(s):  
Xin Wan ◽  
Weiya Pei ◽  
Yiming Zhang ◽  
Lei Zhang ◽  
Khawar Ali Shahzad ◽  
...  
Keyword(s):  
T Cells ◽  
Experimental Autoimmune Encephalomyelitis ◽  
Autoimmune Encephalomyelitis ◽  
Autoreactive T Cells ◽  
And Function ◽  
Experimental Autoimmune

scholarly journals IκB Kinase 2/β Deficiency Controls Expansion of Autoreactive T Cells and Suppresses Experimental Autoimmune Encephalomyelitis

2007 ◽  
Vol 179 (1) ◽  
pp. 179-185 ◽  
Author(s):  
Bernhard Greve ◽  
Robert Weissert ◽  
Nada Hamdi ◽  
Estelle Bettelli ◽  
Raymond A. Sobel ◽  
...  
Keyword(s):  
T Cells ◽  
Experimental Autoimmune Encephalomyelitis ◽  
Autoimmune Encephalomyelitis ◽  
Autoreactive T Cells ◽  
Iκb Kinase ◽  
Experimental Autoimmune

scholarly journals A T cell-intrinsic function for NF-κB RelB in experimental autoimmune encephalomyelitis

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Guilhem Lalle ◽  
Raphaëlle Lautraite ◽  
Allison Voisin ◽  
Julie Twardowski ◽  
Pierre Stéphan ◽  
...  
Keyword(s):  
T Cells ◽  
Experimental Autoimmune Encephalomyelitis ◽  
Clinical Severity ◽  
Autoimmune Encephalomyelitis ◽  
Gm Csf ◽  
Macrophage Colony ◽  
Nf Kappab ◽  
And Function ◽  
Experimental Autoimmune

AbstractNF-kappaB (NF-κB) is a family of transcription factors with pleiotropic functions in immune responses. The alternative NF-κB pathway that leads to the activation of RelB and NF-κB2, was previously associated with the activation and function of T cells, though the exact contribution of these NF-κB subunits remains unclear. Here, using mice carrying conditional ablation of RelB in T cells, we evaluated its role in the development of conventional CD4+ T (Tconv) cells and their function in autoimmune diseases. RelB was largely dispensable for Tconv cell homeostasis, activation and proliferation, and for their polarization toward different flavors of Thelper cells in vitro. Moreover, ablation of RelB had no impact on the capacity of Tconv cells to induce autoimmune colitis. Conversely, clinical severity of experimental autoimmune encephalomyelitis (EAE), a mouse model of multiple sclerosis (MS) was significantly reduced in mice with RelB-deficient T cells. This was associated with impaired expression of granulocyte–macrophage colony-stimulating factor (GM-CSF) specifically in the central nervous system. Our data reveal a discrete role for RelB in the pathogenic function of Tconv cells during EAE, and highlight this transcription factor as a putative therapeutic target in MS.

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