SUMMARYCytokines are important regulators of lymphocyte function in SLE. However, the profile of Th1 and Th2 cytokines produced by circulating lymphocytes in human SLE has not been clearly elucidated. The aim of the present study was to characterize the gene expressions of the Th1-type cytokine IFN-g, and the Th2-type cytokines IL-10 and IL-4 in PBMC of 15 patients with SLE and 10 healthy individuals by a semiquantitative reverse transcriptase polymerase chain reaction (RT-PCR). Our results showed that expression of IFN-g (P 0´0004) and IL-10 (P 0´002) transcripts were significantly increased in PBMC of patients with SLE compared with healthy controls. By contrast, expression of IL-4 transcripts in PBMC of patients with SLE was significantly decreased compared with the healthy controls (P 0´0008). Primary sources of IL-10 were B cells and monocytes, with variable contribution of T cells as detected in various fractions of PBMC of patients with SLE (P 0´049). These findings support the hypothesis that the enhanced production of IFN-g by mononuclear cells may trigger inflammatory responses, together with the enhanced production of IL-10 resulting in autoantibody production by B cells in human SLE.

Humoral immune response seems to play a role in the pathogenesis of multiple sclerosis (MS) and in the central nervous system (CNS) complications of systemic lupus erythematosus (SLE). The aim of the present study was to compare the levels of tumor necrosis factor-alpha (TNF-alpha), interleukin-6 (IL-6) and IL-10 in the cerebrospinal fluid of female patients with several forms of MS (50 patients), and in female patients with several types of CNS complications in SLE (50 patients). Samples were investigated using an enzyme-linked immunosorbent assay technique. Involvement of CNS in SLE patients seems to be characterized with elevated concentrations of all three cytokines in CNS and intrathecal synthesis of IL-6. In MS patients, an intrathecal synthesis of TNF-alpha (relapsing-remitting form) and IL-6 (primary progressive form) were observed. Clinical forms of MS seem to be immunologically heterogeneous. The activation of cytokine network was observed in SLE patients with CNS complications, independent of the pathological process. Similarities between SLE and MS patients with the primary progressive form of the disease were demonstrated concerning the intrathecal synthesis of IL-6. Only MS patients with the relapsing-remitting clinical form showed intrathecal TNF-alpha synthesis.

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Objectives: The aim of the present study was to investigate the role of soluble adhesion molecules in the pathogenesis of multiple sclerosis (MS) and systemic lupus erythematosus (SLE) with demyelinating syndrome. Methods: Paired cerebrospinal fluid (CSF) and serum samples were analysed by an ELISA method to determine the concentrations of sVCAM-1, sICAM-1 and sL-selectin. Intrathecal syntheses of the adhesion molecules were calculated. Results: Elevated serum and CSF concentrations of sVCAM-1 were present in all patient groups. Intrathecal synthesis of sVCAM-1 was present in the relapsing-remitting and secondary progressive forms of MS. Intrathecal synthesis of sICAM-1 was observed in all clinical forms of MS. MS patients with progressive forms of the disease and SLE patients were characterised by intrathecal synthesis of sL-selectin. Conclusions: The data presented suggest that (1) blood-brain barrier damage can be assumed both in systemic disease and organ-specific disease (sVCAM-1), (2) clinical forms of MS differ from each other in respect to concentrations of adhesion molecules and (3) similar immunological events in the central nervous system of SLE patients with demyelinating syndrome and progressive forms of MS can be assumed (sL-selectin).

We observed significantly reduced serum alpha 2-HS glycoprotein concentrations in patients with acute lymphocytic, acute nonlymphocytic, chronic granulocytic and chronic myelomonocytic leukemias, Hodgkin's and non-Hodgkin's lymphomas, myelofibrosis, and multiple myeloma, but not in patients with chronic lymphocytic leukemia and polycythemia vera, as compared with healthy controls. We followed the serum level of the protein for 18 months. Patients with infectious complications, those receiving cytostatic treatment, and those in the preterminal period had further reduced serum alpha 2-HS glycoprotein levels. The reduction of serum alpha 2-HS glycoprotein concentration was primarily due to decreased production caused by infiltration of the liver, a hepatotoxic effect of cytostatic treatment, and, to a lesser degree, to increased consumption. We found statistically significant negative correlations between serum alpha 2-HS glycoprotein concentration and erythrocyte sedimentation rate, serum aspartate aminotransferase and alkaline phosphatase activities, and IgG and IgM concentrations. The determination of the alpha 2-HS glycoprotein concentration is useful for the assessment and follow-up of the clinical status and therapy of patients with hematological malignancies and also has prognostic significance.