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Published on: October 17, 2018
Dendritic cell immunoreceptor regulates Chikungunya virus pathogenesis in mice
Kristin M Long1, Alan C Whitmore, Martin T Ferris
1Department of Genetics, University of North Carolina at Chapel Hill, Chapel Hill, North Carolina, USA.
Journal of Virology
|March 15, 2013
Summary
The dendritic cell immunoreceptor (DCIR) protects against severe Chikungunya virus (CHIKV) disease. DCIR deficiency in mice leads to increased inflammation, tissue damage, and more severe CHIKV symptoms.
Area of Science:
- Immunology
- Virology
- Infectious Diseases
Background:
- Chikungunya virus (CHIKV) causes widespread debilitating illness.
- Alphaviruses interact with C-type lectin receptors.
- Dendritic cell immunoreceptor (DCIR) regulates inflammation and is linked to rheumatoid arthritis.
Purpose of the Study:
- To investigate the role of DCIR in the host response to CHIKV infection.
- To determine if DCIR deficiency exacerbates CHIKV-induced disease.
Main Methods:
- Infection of wild-type C57BL6/J and DCIR-deficient (DCIR(-/-)) mice with CHIKV.
- Analysis of dendritic cell populations and DCIR expression.
- Assessment of cytokine profiles and disease severity (edema, weight loss).
- Histological examination of infected tissues.
Main Results:
- Dendritic cells at CHIKV infection sites showed decreased surface DCIR.
- DCIR(-/-) mice exhibited more severe disease, including rapid edema and weight loss.
- DCIR deficiency led to increased inflammation and joint damage.
- Cytokine responses were altered in DCIR(-/-) mice.
- Early disease severity was independent of viral replication, but later stages showed enhanced inflammation in DCIR(-/-) mice.
Conclusions:
- DCIR plays a protective role in limiting CHIKV-induced inflammation.
- DCIR deficiency exacerbates CHIKV pathogenesis, leading to increased tissue and joint damage.
- Targeting DCIR may offer therapeutic potential for CHIKV infection.
