Antiendotoxin immune response and its relationship to the total immunity and inflammation in patients with systemic lupus erythematosus I and II degree of activity

Shaduro D.V., Beloglazov V.A., Gordienko A.I.

Medical Academy named after S.I .Georgievsky of "Crimean Federal University named after V.I. Vernadsky", Simferopol, Republic of Crimea, Russia

The aim of this study was to investigate the influence and correlation of cellular and humoral antiendotoxin immune response to common immunity and systemic inflammation indicators in systemic lupus erythematosus (SLE) patients with different degrees of activity.
Materials and methods. The studied group consisted of 48 patients with SLE (I degree - 27, II- 21), control group - 40 relatively healthy donor. Design of the study was to determine the level and amount of major subpopulations of lymphocytes (CD3+, CD19+, CD4+, CD8+, CD3+ HLADR, CD3+ / 16 + / 56 +, CD3-/16 +56 +), expression of receptors CD14 and LPS-FITC, phagocytic activity of neutrophils, the overall concentration of immunoglobulins and specific anti-endotoxin antibody class A, M and the G, circulating immune complexes, C-reactive protein, endogenous intoxication. A study was performed by flow laser cytometry, spectrophotometry, ELISA.
Results. SLE patients revealed dysfunction of both humoral and cellular immune response antiendotoxin in reduction of expression of CD14 and LPS-FITC receptors (25% and 14%, respectively) and sharp increase in anti-endotoxin class G antibodies (more than 2 fold). Revealed changes grow up with increasing of disease activity. The observed correlations between endotoxin immune response and the overall immune status, as well as with systemic inflammation indicators confirm the close relationship and the impact intensity of this type of immune response and systemic inflammation, in fast, the most pronounced relations were found in patients with a low degree of SLE activity.
Conclusions. The presence of the identified antiendotoxin immune response dysfunction is amplified with an increase in disease activity, reflecting the persistent influence of LPS on cellular LPS-binding system in SLE patients.