Immune Netw.  2012 Apr;12(2):48-57. 10.4110/in.2012.12.2.48.

The Roles and Perspectives of Toll-Like Receptors and CD4+ Helper T Cell Subsets in Acute Viral Encephalitis

Affiliations
  • 1College of Veterinary Medicine and Bio-Safety Research Institute, Chonbuk National University, Jeonju 561-756, Korea. vetvirus@chonbuk.ac.kr
  • 2Laboratory of Neurovirology and Inflammation Biology, Centre for Cellular and Molecular Biology, Uppal Road, Hyderabad-07, India.

Abstract

Acute viral encephalitis caused by neurotrophic viruses, such as mosquito-borne flaviviruses, is an emerging and re-emerging disease that represents an immense global health problem. Considerable progression has been made in understanding the pathogenesis of acute viral encephalitis, but the immune-pathological processes occurring during the progression of encephalitis and the roles played by various molecules and cellular components of the innate and adaptive systems still remain undefined. Recent findings reveal the significant contribution of Toll-like receptors (TLRs) and regulatory CD4+ T cells in the outcomes of infectious diseases caused by neurotrophic viruses. In this review, we discuss the ample evidence focused on the roles of TLRs and CD4+ helper T cell subsets on the progression of acute viral encephalitis. Finally, we draw attention to the importance of these molecules and cellular components in defining the pathogenesis of acute viral encephalitis, thereby providing new therapeutic avenues for this disease.

Keyword

Toll-like receptors; CD4+ Th subsets; Acute viral encephalitis; Japanese encephalitis virus; West Nile virus; Dengue virus

MeSH Terms

Communicable Diseases
Dengue Virus
Encephalitis
Encephalitis Virus, Japanese
Encephalitis, Viral
Flavivirus
T-Lymphocyte Subsets
T-Lymphocytes
Toll-Like Receptors
West Nile virus
Toll-Like Receptors

Figure

  • Figure 1 IL-6 may be a key molecule in regulating the balance of differentiation between CD4+Foxp3+ Treg and IL-17+RORγt+ Th17 cells.


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