AI Article Synopsis

  • C57BL/6 mice are genetically modified to study autoimmune arthritis, specifically collagen-induced arthritis, despite being resistant to it.
  • The study involved immunising these mice with type II collagen and comparing their arthritis development and drug response to DBA/1 mice.
  • Results indicated that C57BL/6 mice develop a milder form of arthritis that responds similarly to rheumatoid arthritis, making them a useful model for researching arthritis-related genes and testing new treatments.

Article Abstract

Many genetically modified mouse strains are now available on a C57BL/6 (H-2b) background, a strain that is relatively resistant to collagen-induced arthritis. To facilitate the molecular understanding of autoimmune arthritis, we characterised the induction of arthritis in C57BL/6 mice and then validated the disease as a relevant pre-clinical model for rheumatoid arthritis. C57BL/6 mice were immunised with type II collagen using different protocols, and arthritis incidence, severity, and response to commonly used anti-arthritic drugs were assessed and compared with DBA/1 mice. We confirmed that C57BL/6 mice are susceptible to arthritis induced by immunisation with chicken type II collagen and develop strong and sustained T-cell responses to type II collagen. Arthritis was milder in C57BL/6 mice than DBA/1 mice and more closely resembled rheumatoid arthritis in its response to therapeutic intervention. Our findings show that C57BL/6 mice are susceptible to collagen-induced arthritis, providing a valuable model for assessing the role of specific genes involved in the induction and/or maintenance of arthritis and for evaluating the efficacy of novel drugs, particularly those targeted at T cells.

Download full-text PDF

Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2212575PMC
http://dx.doi.org/10.1186/ar2319DOI Listing

Publication Analysis

Top Keywords

c57bl/6 mice
24
type collagen
16
collagen-induced arthritis
12
arthritis c57bl/6
12
arthritis
10
mice
8
sustained t-cell
8
rheumatoid arthritis
8
dba/1 mice
8
mice susceptible
8

Similar Publications

Longitudinal single-cell RNA sequencing reveals a heterogeneous response of plasma cells to colonic inflammation.

Int J Biol Macromol

January 2025

Department of Physiology, School of Basic Medical Sciences, Department of Colorectal Surgery, Qilu Hospital, Cheeloo College of Medicine, Shandong University, Jinan, Shandong 250012, China. Electronic address:

A comprehensive understanding of the dynamic changes in plasma cells (PCs) during inflammation remains elusive. In this study, we analyzed the distinct responses of PCs across different phases of inflammation in a dextran sodium sulfate (DSS)-induced mouse colitis model. Six-week-old male C57BL/6 mice were treated with 2.

View Article and Find Full Text PDF

Dual efficacy of tocilizumab in managing PD-1 inhibitors-induced myocardial inflammatory injury and suppressing tumor growth with PD-1 inhibitors: a preclinical study.

Cancer Immunol Immunother

January 2025

Department of Oncology, The Second Affiliated Hospital, Jiangxi Medical College, Nanchang University, Nanchang, 330006, Jiangxi Province, China.

The combined use of tocilizumab (TCZ) and immune checkpoint inhibitors (ICIs) in cancer treatment is gaining attention, but preclinical studies are lacking. Our study aims to investigate the synergistic anti-tumor effect of TCZ combined with ICIs and its role in treating immune-related adverse events (irAEs). The clinical significance of high interleukin-6 (IL-6) expression in tumor patients was analyzed from the Cancer Genome Atlas (TCGA) database.

View Article and Find Full Text PDF

The negative impact of repeated-mild traumatic brain injury (rmTBI) is profoundly seen in circadian-disrupted individuals. The unrelenting inflammation, glial activation, and gut dysbiosis are key neuropathological aberrations in the aftermath of rmTBI. In this study, we examined the impact of chitosan lactate (CL) on circadian disturbance (CD) + rmTBI-generated neurological dysfunctions and its prebiotic response on the gut-brain axis.

View Article and Find Full Text PDF

Osteogenesis imperfecta (OI) is an inheritable skeletal disorder characterized by bone fragility often caused by pathogenic variants in the COL1A1 gene. Current OI mouse models with a glycine substitution in Col1a1 exhibit excessive severity, thereby limiting long-term pathophysiological analysis and drug effect assessments. To address this limitation, we constructed a novel OI mouse model mimicking a patient with OI type III.

View Article and Find Full Text PDF

Background: Compelling evidence has shown that long non-coding RNAs (lncRNAs) contribute to Alzheimer's disease (AD) pathogenesis including β-amyloid plaque deposition (Aβ) and intracellular neurofibrillary tangles. In this study, we aimed to investigate the critical role of lncRNA Gm20063 in AD.

Method: Six-month-old male APP/PS1 transgenic mice and wild type (WT) C57BL/6 (B6) littermates were obtained from the Nanjing University Animal Model Research Center.

View Article and Find Full Text PDF

Want AI Summaries of new PubMed Abstracts delivered to your In-box?

Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!