The Endoplasmic Reticulum Stress-Inducible Protein, Herp, Is a Potential Triggering Antigen for Anti-DNA Response

Hirabayashi, Yasuhiko; Oka, Yasu; Ikeda, Tomoko; Fujii, Hiroshi; Ishii, Tomonori; Sasaki, Takeshi; Harigae, Hideo

doi:10.4049/jimmunol.0900670

Cited by 17 publications

(17 citation statements)

References 48 publications

(40 reference statements)

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Immunization of normal BALB/c mice with Herp elicited anti-dsDNA Abs and caused glomerular IgG deposition [62]. However, urinary protein level did not increase and overt nephritis did not develop.…”

Section: Antigenicity Of Herp For Anti-dsdna Ab Production In Micementioning

confidence: 97%

“…The production of Herp is induced by endoplasmic reticulum (ER) stress. The PBLs from subjects in active SLE, especially at the time of onset or flare-up of the disease, tended to show Herp expression [62]. The expression of Herp was also observed in the lymph node of an untreated patient with active SLE, indicating that Herp can be exposed to the immune system in lymph nodes where Ag recognition occurs (Figure 1).…”

Section: Cross-reactive Antigen Of the O-81 Human Nephritogenic Anti-mentioning

confidence: 97%

“…We found that the O-81 Ab specifically cross-reacts with human homocysteine-induced endoplasmic reticulum protein (Herp) [62]. Anti-dsDNA Abs purified from the sera of SLE patients bound to Herp, and anti-Herp Abs purified from the sera of SLE bound to dsDNA [62].…”

Section: Cross-reactive Antigen Of the O-81 Human Nephritogenic Anti-mentioning

confidence: 99%

“…Anti-dsDNA Abs purified from the sera of SLE patients bound to Herp, and anti-Herp Abs purified from the sera of SLE bound to dsDNA [62]. The production of Herp is induced by endoplasmic reticulum (ER) stress.…”

Section: Cross-reactive Antigen Of the O-81 Human Nephritogenic Anti-mentioning

confidence: 99%

“…Herp can be exposed on apoptotic blebs of ER stress-induced apoptotic cells [62]. Many apoptotic cells expressing Herp were observed in the peripheral blood mononuclear cells (PBMCs) of patients with active SLE, but not normal control subjects [62].…”

Section: Cross-reactive Antigen Of the O-81 Human Nephritogenic Anti-mentioning

confidence: 99%

See 4 more Smart Citations

Cell Death and Anti-DNA Antibodies

Hirabayashi¹

2012

Apoptosis and Medicine

Self Cite

View full text Add to dashboard Cite

Section: Antigenicity Of Herp For Anti-dsdna Ab Production In Micementioning

confidence: 97%

Section: Cross-reactive Antigen Of the O-81 Human Nephritogenic Anti-mentioning

confidence: 97%

Section: Cross-reactive Antigen Of the O-81 Human Nephritogenic Anti-mentioning

confidence: 99%

Section: Cross-reactive Antigen Of the O-81 Human Nephritogenic Anti-mentioning

confidence: 99%

Section: Cross-reactive Antigen Of the O-81 Human Nephritogenic Anti-mentioning

confidence: 99%

See 3 more Smart Citations

Cell Death and Anti-DNA Antibodies

Hirabayashi¹

2012

Apoptosis and Medicine

Self Cite

View full text Add to dashboard Cite

Endoplasmic Reticulum Stress Interacts With Inflammation in Human Diseases

Cao

Luo

Shi

2015

Journal Cellular Physiology

131

View full text Add to dashboard Cite

The endoplasmic reticulum is a critical organelle for normal cell function and homeostasis. Disturbed protein folding process in the ER, termed ER stress, leads to the activation of unfolded protein response (UPR) that encompasses a complex network of intracellular signaling pathways. The UPR can either restore ER homeostasis or activate pro-apoptotic pathways depending on specific insults, intensity and duration of the stress, and cell types. ER stress and the UPR have recently been linked to inflammation in a variety of human pathologies including autoimmune diseases, infection, neurodegenerative disease, and metabolic disorders. In the cell, ER stress and inflammatory signaling share extensive regulators and effectors in a broad spectrum of biological processes. In spite of different etiologies, the two signaling pathways were shown to form a vicious cycle in exacerbating cellular dysfunction and causing apoptosis in many cells and tissues. However, the interaction between ER stress and inflammation in many of these diseases remains elusive. Further understanding of those issues may enable the development of novel therapies that spontaneously target these pathogenic pathways.

show abstract