scholarly journals Systemic autoimmune disease induced by dendritic cells that have captured necrotic but not apoptotic cells in susceptible mouse strains

2005 ◽  
Vol 35 (11) ◽  
pp. 3364-3375 ◽  
Author(s):  
Liang Ma ◽  
Kwok-Wah Chan ◽  
Nigel J. Trendell-Smith ◽  
Adrian Wu ◽  
Lina Tian ◽  
...  
Keyword(s):  
Dendritic Cells ◽  
Autoimmune Disease ◽  
Mouse Strains ◽  
Systemic Autoimmune Disease ◽  
Apoptotic Cells ◽  
Susceptible Mouse

scholarly journals Transcriptional Remodeling Patterns in Murine Dendritic Cells Infected with Paracoccidioides brasiliensis: More Is Not Necessarily Better

2020 ◽  
Vol 6 (4) ◽  
pp. 311
Author(s):  
Calliandra M. de-Souza-Silva ◽  
Fabián Andrés Hurtado ◽  
Aldo Henrique Tavares ◽  
Getúlio P. de Oliveira ◽  
Taina Raiol ◽  
...  
Keyword(s):  
Dendritic Cells ◽  
Resistant Strain ◽  
Antigen Processing ◽  
Paracoccidioides Brasiliensis ◽  
Adaptive Immune Response ◽  
Susceptible Strain ◽  
Mouse Strains ◽  
Sequencing Analysis ◽  
Susceptible Mouse ◽  
Antigen Processing And Presentation

Most people infected with the fungus Paracoccidioides spp. do not get sick, but approximately 5% develop paracoccidioidomycosis. Understanding how host immunity determinants influence disease development could lead to novel preventative or therapeutic strategies; hence, we used two mouse strains that are resistant (A/J) or susceptible (B10.A) to P. brasiliensis to study how dendritic cells (DCs) respond to the infection. RNA sequencing analysis showed that the susceptible strain DCs remodeled their transcriptomes much more intensely than those from the resistant strain, agreeing with a previous model of more intense innate immunity response in the susceptible strain. Contrastingly, these cells also repress genes/processes involved in antigen processing and presentation, such as lysosomal activity and autophagy. After the interaction with P. brasiliensis, both DCs and macrophages from the susceptible mouse reduced the autophagy marker LC3-II recruitment to the fungal phagosome compared to the resistant strain cells, confirming this pathway’s repression. These results suggest that impairment in antigen processing and presentation processes might be partially responsible for the inefficient activation of the adaptive immune response in this model.

Necrotic Cells Induce Systemic Autoimmune Disease in vivo by Activation of Dendritic Cells (DCs)

2005 ◽  
Vol 115 (4) ◽  
pp. 891 ◽  
Author(s):  
L. Ma ◽  
K. Chan ◽  
N. Trendell-Smith ◽  
C. Lo ◽  
C. To ◽  
...  
Keyword(s):  
Dendritic Cells ◽  
Autoimmune Disease ◽  
Systemic Autoimmune Disease

No Zinc Deficiency But a Putative Immunosuppressive Role for Labile Zn in Patients with Systemic Autoimmune Disease

2017 ◽  
Vol 13 (1) ◽  
pp. 59-64 ◽  
Author(s):  
Johannes Nossent ◽  
Sue Lester ◽  
Maureen Rischmueller ◽  
Peter Zalewski
Keyword(s):  
Autoimmune Disease ◽  
Zinc Deficiency ◽  
Systemic Autoimmune Disease

scholarly journals Dysregulated expression of the T cell cytokine Eta-1 in CD4-8- lymphocytes during the development of murine autoimmune disease.

1990 ◽  
Vol 172 (4) ◽  
pp. 1177-1183 ◽  
Author(s):  
R Patarca ◽  
F Y Wei ◽  
P Singh ◽  
M I Morasso ◽  
H Cantor
Keyword(s):  
T Cell ◽  
B Cells ◽  
Autoimmune Disease ◽  
Cell Activation ◽  
Cell Clone ◽  
Inbred Mouse ◽  
Inbred Mouse Strain ◽  
Mouse Strains ◽  
Effector Cells ◽  
T Cell Clone

The development of autoimmune disease in the MRL/MpJ-lpr inbred mouse strain depends upon the maturation of a subset of T lymphocytes that may cause sustained activation of immunological effector cells such as B cells and macrophages. We tested the hypothesis that abnormal effector cell activation reflects constitutive overexpression of a T cell cytokine. We found that a newly defined T cell cytokine, Eta-1, is expressed at very high levels in T cells from MRL/l mice but not normal mouse strains and in a CD4-8- 45R+ T cell clone. The Eta-1 gene encodes a secreted protein that binds specifically to macrophages, possibly via a cell adhesion receptor, resulting in alterations in the mobility and activation state of this cell type (Patarca, R., G. J. Freeman, R. P. Singh, et al. 1989. J. Exp. Med. 170:145; Singh, R. P., R. Patarca, J. Schwartz, P. Singh, and H. Cantor. 1990. J. Exp. Med. 171:1931). In addition, recent studies have indicated that Eta-1 can enhance secretion of IgM and IgG by mixtures of macrophages and B cells (Patarca, R., M. A. Lampe, M. V. Iregai, and H. Cantor, manuscript in preparation). Dysregulation of Eta-1 expression begins at the onset of autoimmune disease and continues throughout the course of this disorder. Maximal levels of Eta-1 expression and the development of severe autoimmune disease reflect the combined contribution of the lpr gene and MRL background genes.

scholarly journals NK Cell Activation in the Antitumor Response Induced by IFN-α Dendritic Cells Loaded with Apoptotic Cells from Follicular Lymphoma Patients

2016 ◽  
Vol 197 (3) ◽  
pp. 795-806 ◽  
Author(s):  
Caterina Lapenta ◽  
Simona Donati ◽  
Francesca Spadaro ◽  
Paolo Castaldo ◽  
Filippo Belardelli ◽  
...  
Keyword(s):  
Dendritic Cells ◽  
Follicular Lymphoma ◽  
Cell Activation ◽  
Nk Cell ◽  
Apoptotic Cells ◽  
Antitumor Response
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