Galina A. Chudilova

By Irina V. Nesterova, Galina A. Chudilova, Svetlana V. Kovaleva, Lyudmila V. Lomtatidze and Tatyana V. Rusinova

Neutrophilic granulocytes (NGs) are very important cells of innate immunity that can very quickly realize antibacterial and antiviral defense. Until the present time, the phenomenon of different levels of presentations of membrane receptors CD16 and CD11b NG in normal and pathological conditions wasn’t studied. We had studied the population of CD16+CD11b+NG in two groups of patients with acute viral and acute bacterial infections in the models of acute bacterial tonsillitis (ABT) and acute viral tonsillitis-EBV infection (AEBVI), having the same clinical symptoms in early stages of the disease. Comparative analysis of the redistribution of equipment intensity of CD16 and CD11b has detected three subpopulations of CD16+CD11b+NG population—CD16brightCD11bbright, CD16brightCD11bdim, and CD16dimCD11bbright—in normal and pathological conditions. It was found that subpopulation CD16brightCD11bdimNG dominates in healthy individuals; subpopulation CD16brightCD11bbrightNG dominates in patients with acute viral infection; subpopulation CD16dimCD11bbrightNG dominates in patients with acute bacterial infections. We had demonstrated that the study of CD16+CD11b+NG subpopulations allows in early stage of diseases to diagnose acute viral and acute bacterial infections. Our studies have demonstrated the positive effects of eukaryotic DNA sodium salt on the negatively altered phenotype subpopulation CD16+CD11b+NG, in particular, through the remodeling of the expression of CD11b on NG membrane.

Part of the book: Neutrophils

By Irina V. Nesterova, Svetlana V. Kovaleva, Valentina V. Malinovskaya, Galina A. Chudilova and Tatyana V. Rusinova

This chapter reviews various interferon (IFN) system disturbances—interferonopathies. The authors describe clinical specifics of type I interferonopathy associated with overexpression of IFNα—which is a rare Mendelian genetic disease. Certain autoimmune diseases (systemic lupus erythematosus (SLE), vasculitis, immune dysregulation syndrome, etc.) are also characterized by overproduction of IFNα. Furthermore the most common interferonopathies are described—deficiencies of IFN, congenital or acquired IFNα/IFNβ and IFNγ deficiencies in children and adults. Deficiency of IFNα/IFNβ associated with severe recurrent viral infections and deficiency of IFNγ cause mycobacterial infection. Interferon-corrective therapy methods are described. The target therapy of type I interferonopathies (biologics) binds IFNα and normalizes the high level of IFNα. From the other side, patients with congenital IFNα deficiencies are needed in replacement IFN therapy. In case of acquired IFNα deficiency, the differentiated interferon-corrective therapy is performed. In both replacement and interferon-corrective therapies, recombinant human IFNα2b in complex with antioxidants (Viferon®) can be used, because their application is safe and has good clinical efficiency and no side effects.

Part of the book: Innate Immunity in Health and Disease