scholarly journals OP0313 P75 low affinity receptor of nerve growth factor on peripheral leukocytes and cd11c-positive dendritic cells are upregulated in patients with systemic lupus erythematosus

Author(s):  
S Welle ◽  
AM Wolf ◽  
MF Seidel
Lupus ◽  
2020 ◽  
Vol 29 (8) ◽  
pp. 970-975 ◽  
Author(s):  
Stefanie Welle ◽  
Anna M Wolf ◽  
Christian Dernbach ◽  
Ute Klarmann-Schulz ◽  
Matthias F Seidel

Introduction The nervous system modulates rheumatic diseases in neurogenic inflammation (NI). Nerve growth factor (NGF) plays a pivotal role in NI and chronic nociceptive pain. However, the role of NGF in autoimmune inflammatory diseases is not well understood. The aim of this study was to analyse NGF high- (TrkA) and low-affinity (p75) receptors on all major leucocyte subsets of patients with systemic lupus erythematosus (SLE) as a potential indicator of NI. Methods A total of 13 patients were analysed by fluorescence-activated cell sorting and compared to 13 healthy control (HC) subjects. Patients were also stratified for high or low disease activity (CRP, ESR, SLEDAI, ANA, anti-dsDNA and C3/C4). Statistics included the Kruskal–Wallis test and Mann–Whitney U-test. Results When comparing patients and HC, TrkA was not differentially expressed. In contrast, p75 was increased on CD16+ and CD56+ leucocytes in patients. CD11c+ dendritic cells (DC) were in total increased in SLE. DCs were also significantly elevated in active patients. Furthermore, we found an intermediate CD11b+ population strongly expressing TrkA in patients and HC. Conclusion We demonstrate for the first time differential NGF receptor expression in SLE. The increased CD11c+ DCs might indicate additional activation in SLE.


1996 ◽  
Vol 204 (1-2) ◽  
pp. 13-16 ◽  
Author(s):  
Luisa Bracci-Laudiero ◽  
Thomas Lundeberg ◽  
Carina Stenfors ◽  
Elvar Theodorsson ◽  
Paola Tirassa ◽  
...  

Cytokine ◽  
2002 ◽  
Vol 20 (3) ◽  
pp. 136-139 ◽  
Author(s):  
Kristiina Aalto ◽  
Laura Korhonen ◽  
Pekka Lahdenne ◽  
Pirkko Pelkonen ◽  
Dan Lindholm

2012 ◽  
Vol 71 (Suppl 1) ◽  
pp. A34.1-A34
Author(s):  
Ahsen Morva ◽  
Sébastien Lemoine ◽  
Achouak Achour ◽  
Alain Saraux ◽  
Jacques-Olivier Pers ◽  
...  

2015 ◽  
Vol 112 (45) ◽  
pp. E6195-E6204 ◽  
Author(s):  
Teja Celhar ◽  
Richard Hopkins ◽  
Susannah I. Thornhill ◽  
Raquel De Magalhaes ◽  
Sun-Hee Hwang ◽  
...  

Glomerulonephritis is a common and debilitating feature of systemic lupus erythematosus (SLE). The precise immune mechanisms that drive the progression from benign autoimmunity to glomerulonephritis are largely unknown. Previous investigations have shown that a moderate increase of the innate Toll-like receptor 7 (TLR7) is sufficient for the development of nephritis. In these systems normalization of B-cell TLR7 expression or temporal depletion of plasmacytoid dendritic cells (pDCs) slow progression; however, the critical cell that is responsible for driving full immunopathology remains unidentified. In this investigation we have shown that conventional DC expression of TLR7 is essential for severe autoimmunity in the Sle1Tg7 model of SLE. We show that a novel expanding CD11b+ conventional DC subpopulation dominates the infiltrating renal inflammatory milieu, localizing to the glomeruli. Moreover, exposure of human myeloid DCs to IFN-α or Flu increases TLR7 expression, suggesting they may have a role in self-RNA recognition pathways in clinical disease. To our knowledge, this study is the first to highlight the importance of conventional DC-TLR7 expression for kidney pathogenesis in a murine model of SLE.


Sign in / Sign up

Export Citation Format

Share Document