The possible role of T cell and macrophage in development of Behcet's disease-like symptoms induced by herpes simplex virus in ICR mice

Abstract

Although the etiology of Behcet´s disease is unclear, viral infection has long been postulated as being one of the factors. We already reported the presence of herpes simplex virus (HSV) DNA in salivas, intestinal mucosa, and genital mucosa from patients with Behcet´s disease using polymerase chain reaction (PCR). We have also been able to induce Behcet´s disease-like symptoms in ICR mice by inoculation of HSV4 However, HSV alone is not sufficient to explain the pathogenesis of Behcet´s disease. There are some evidences to suggest that immunological abnormalities are important with its pathogenesis. A disturbance in circulating T cell function was found initially in a small decrease in CD4 cells and a defect in suppressor functions The mucocutaneous lesions of Behcet´s disease were initially infiltrated with CD4, CD8 cells, macrophages and dendritic cells followed by neutrophils. However, more recently, attention has focused on TH1 and TH2 cytokines generated by T cells. 4 mixed pattern of THI and TH2 was observed, probably with a significant contribution from macrophages To study the possible relationship between immune regulation and induction of Behcet´s disease-like symptoms, inactivation or activation of T lymphocytes or macrophages before and/or after inoculation of HSV was necessary. It has been reported that long-term treatment with silica or anti-macl or anti-mac2 monoclonal antibody may cause macrophage depletion or inactivation. Also treatment with anti-CD4 or anti-CD8 monoclonal antibody may cause T cell inactivation or depletionlo.11. As an initial step of inactivation experiment, we have used several monoclonal antibodies against macrophages and T lymphocytes to inactivate T cells and macrophages followed by HSV inoculation in ICR mice to see whether they might play a certain role in the pathogenesis of Behcet´s disease.