Abstract
Introduction: Reactivation of human herpesviruses (HHV-6, HHV-7, EBV) is considered to be one of the factors capable of modifying the course of systemic immuno-inflammatory diseases through their influence on immune regulatory mechanisms.
Objective: To assess the characteristics of the regulatory and effector components of cellular immunity in patients with virus-associated systemic lupus erythematosus (SLE) and secondary systemic vasculitides in the context of active herpesvirus replication.
Materials and Methods: Thirty-nine patients aged 18-68 with PCR-confirmed presence of HHV-6, HHV-7 or EBV in peripheral blood were examined: 22 patients with virus-associated SLE and 17 patients with secondary systemic vasculitides. The control group consisted of 20 apparently healthy individuals, matched for age and sex. Immunophenotyping was performed using multiparametric flow cytometry to identify the subpopulations of CD3+, CD4+, CD8+, CD4+CD45RO+, CD3+HLA-DR+, TNK-, NK cells and regulatory T cells (CD45+CD4+CD25^bright^CD127^neg^).
Results: In patients with SLE, a reduction in the proportion of lymphocytes (20.9% [17.6–24.8]) and the lymphocyte/granulocyte ratio (0.29 [0.22–0.36]) were observed in patients with SLE, in conjunction with an increase in the proportion of TNK-cells (9.2% [7.4–11.6]; p=0.003). The level of regulatory T-cells was reduced in both clinical groups compared with the control group (7–10%), but was more pronounced in SLE (4.1%) than in vasculitides (5.9%). Secondary vasculitides were characterized by signs of enhanced adaptive immune activation, in particular an increase in the proportion of CD4+ memory cells and CD4+HLA-DR+ lymphocytes.
Conclusions: Under identical conditions of active herpesvirus replication, different immunological phenotypes develop. SLE is characterized by a more profound deficit in the regulatory T-cell component and signs of cytotoxic activation, whereas secondary vasculitides are associated with a predominance of the adaptive T-cell response. The data obtained suggest a possible role for herpesviruses in the development of immune dysregulation in systemic autoimmune diseases. Given the limited sample size, the results should be regarded as preliminary and in need of confirmation in larger prospective studies.