Mesenchymal stromal or stem cells (MSC) represent a population of primitive fibroblastlike cells that are able to differentiate into cellular lineages of connective tissue (osteocytes, chondrocytes, adipocytes), skeletal muscles, and blood vessels. The review deals with contemporary views concerning descent, immunophenotype and immunogenicity of MSC. The studies over last decade revealed an ability of MSC to function as immunomodulatory populations which may suppress innate immunity factors (dendritic cells, natural killers, complement), as well as T-helpers and cytotoxic T-lymphocytes, along with activation of regulatory T lymphocytes (Treg). Special attention is given to analysis of conflicting data about influence of MSC on functions of B-lymphocytes and plasma cells in experimental settings, both in vitro and in vivo conditions. Data presently available are insufficient to explain the controversions revealed. In future investigations, it is necessary to consider attribution of B-cells to B1a, B1b, or B2 subpopulations as well as possible presence of poorly studied regulatory B-cells. It is also important also to take into account potential heterogeneity of initial MSC populations being isolated according to previously approved protocols. (Med. Immunol., 2014, vol. 16, N 2, pp 107-126)

Significance of psoriasis (PS) research is determined by increasing incidence of this disorder, higher frequency of severe clinical forms, e.g., psoriatic arthritis (PsA). Clinical course and outcomes of psoriasis and psoriatic arthritis depend on degree of immunological disturbances and imbalance of cytokine regulation of intercellular interactions. The leading immune disorders involved in pathogenesis of psoriasis and PsA are those characterized by alterations of Th1-type cytokine profile (TNFα, IL-2, IFNγ, etc.). We have analyzed publications that reveal some features of PS and PsA immunopathogenesis associated with nature of the diseases. The review draws attention to relatively new and scarcely studied data concerning the role of cytokines produced by Th17- and Th22-cells (IL-17, IL-22, IL-23, IL-26), IL-19 subfamily (IL-19, IL-20, IL-24) in development of psoriasis and PsA. Search for the immunological markers predisposing for risk of psoriasis and PsA is an important step in personalized approach to their prediction and planning of preventive measures, in order to prevent progression of this pathology.

The aim of present work was to evaluate the effect of mesenchymal stromal cells (MSCs) from lymphoma patients on the in vitro and in vivo homeostatic proliferation of lymphocytes. Our data have demonstrated
for the first time, that MSCs from lymphoma patient are able to enhance the in vitro proliferation of donor and patient mononuclear cells (MNCs) in response to IL-2 or IL-7. This effect was observed within a wide range
of MSC-to-MNC ratios (1:50-1:2). Lymphocyte reactivity to IL-2 or IL-7 was found to be an important factor determining the stimulatory effect of MSCs. Ex vivo studies in the patients undergoing autologous hematopoietic stem cell transplantation (AHSCT) have shown that the patients co-transplanted with MSCs exhibited higher proportions of proliferating CD8+T cells (especially, memory cells) at the day of engraftment, than before AHSCT, as compared to the patients subjected to standard AHSCT protocols. Moreover, there was no an increase in apoptosis of naive CD4+T cells that was typical for standard AHSCT. These data indicate that the stimulatory effect of MSCs upon T lymphocyte proliferation following chemotherapy-induced lymphopenia
concerns, mainly, the memory CD8+T cell population, whereas more efficient recovery of naive CD4+T cells is due to anti-apoptotic effects of MSCs.

We observed sixty patients with allergic bronchial asthma (ABA) and 54 with non-allergic bronchial asthma (NABA). Quantitative SOCS3 and SOCS5 mRNA expression was evaluated by means of real-time PCR. Eighteen healthy persons served as a control group. In patients with bronchial asthma (irrespectively of pathogenetic form), a significant increase of SOCS3 transcription factor expression was detected in peripheral blood mononuclears, as compared with control group. This increase was more pronounced in NABA group. The mRNA SOCS5 level was significantly decreased in bronchial asthma patients, as compared to control group, especially, in ABA subgroup rather than in NABA patients. Thus, an increased expression of SOCS3 mRNA in BA patients could be regarded as a protective antiinflammatory response Decrease of SOCS5 mRNA expression in patients with bronchial asthma (being more pronounced in ABA), may be indicative for a deficiency in negative feedback regulation of gene transcription in allergic bronchial asthma.

Taking into account interrelations between inflammation and hemostasis, as well as immediate effects of IL-1β, IL-6 and TNFα upon blood coagulation system, one may suggest that their functional variants
could determine thrombosis risks both in arterial and venous circulation. The aim of this study was to assess possible role of allelic IL-1β, IL-6 and TNFα variants in pathogenesis of venous thromboembolism (VTE)
in young patients. A retrospective analysis was performed for a group of 180 patients with early-onset VTE, and 150 healthy. In a sub-group with deep-vein thrombosis of lower extremities (DWTLE) complicated by
pulmonary artery thromboembolia (PAT), we have revealed increased frequencies of IL-6 –174C homozygotes (30.8% vs 13.0%, p = 0.02) and IL-1β –31Т (61.5% vs 40.9%, p = 0.03), when compared with a subgroup of DWTLE. Among patients with “isolated” PAT a tendency for increased IL-1β –31ТТ ratio was found, as compared with DWTLE (53.8% vs 40.9%, р = 0,3), like as with control group (53.8% vs 40.7%, р = 0,3), These differences, however, were statistically insignificant. These data may suggest certain effects of IL-1β and IL-6 gene polymorphisms upon clinical characteristics of venous thromboembolism, rather than upon general VTE risk among young persons.

Periodontitis is a chronic infectious inflammatory disease, being the most common bone disease in humans. Porphyromonas gingivalis bacteria are quite common in periodontal lesions, thus considered among major causal agents of periodontitis. Monocytes play a crucial role in development of the infectious events and subsequent inflammation. The aim of this study was to investigate appropriate changes of the monocyte subpopulations, as well as to assess relationships between expression of CD14, CD16, CD45RA, HLA-DR on the monocyte surfaces in the patients with periodontitis. It was demonstrated that periodontitis is accompanied by increased counts of pro-inflammatory monocytes. These changes are characterized by decreased expression of CD14, along with occurence of CD16 marker. Concomitant activation of the monocytes is reflected by CD45RA expression. However, in spite of significant increase in CD14lowCD16+HLA-DR+ cell counts observed in patients with periodontitis, these monocyte populations are not likely to play a significant role in development of a specific immune response and suppression of periodontitis.

Acute sepsis (1-3 days after admission) has been compared with tertiary peritonitis, as a clinical variant of prolonged sepsis (7 to 42 days after admission). A total of 153 patients were enrolled into the study, including 112 cases of multiple organ dysfunction syndrome (MODS, as assessed by SOFA score), of them thirty-one with septic shock; fatal outcomes, in 48 cases. Plasma concentrations of C-reactive protein, cytokines (IL-6, IL-8, IL-10, TNFα), cortisol, troponin I, myoglobin, D-dimer were detected by means of immunochemiluminesce assay (ImmuLite). Development of systemic inflammation (SI) was evaluated by appropriate integral criteria. An association was established between SI development and critical complications in the both groups of patients. Meanwhile, hyperergic variants of SI development associated with high cytokine levels, proved to prevail in acute sepsis. On the contrary, hypoergic variants were more common in cases of tertiary peritonitis, being characterized by relatively low levels of cytokines, along with higher probability of other SI syndromes and risks of lethal outcomes. In summary, systemic inflammatory events in acute versus prolonged sepsis may proceed by different pathogenetic pathways.

It was found that soluble intercellular adhesion molecule-1 (ICAM-1) and leukocyte levels in patients with non-ST elevation acute coronary syndrome exhibited a gradual decrease during follow-up period of 6 to 12 months after CABG, as compared with pre-treatment baseline rates. In addition, sICAM-1 level showed an increase at 48 month post-CABG, tending to pre-treatment values. The levels of tumor necrosis factor-alpha (TNFa) and interleukin-6 (IL-6) did not express any significant changes during the entire observation period. TNFα level in the patients with non-STEMI before surgery did not differ from the levels in the patients with stable ischemic heart disease (60.0±9.8 pg/ml and 51.0±6.8 pg/ml; p > 0.05). Serum TNFα level remained unchanged in the patients after CABG. Similar changes were found for IL-6, with no differences between initial levels in the patients with non-STEMI and those with stable coronary artery disease (34.5±3.6 pg/ml and 28.6±3.1 pg/ml; p > 0.05). The IL-6 levels remained virtually unchanged over the observation time. Therefore, the ambiguous results obtained in present study deserve further studies of the role of inflammatory mediators in different clinical forms of ischemic heart disease following CABG.

Chemokines are believed to play an important role in immunopathogenesis of different joint diseases. One of important problems in studies of synovial fluid is determination of normal level of chemokines from control patients. In our study we determined concentrations of number of chemokines in relatively normal synovial fluid from subjects with background traumatic joint injury without systemic or local inflammation at the moment of study. Results for several CC- and CXC-chemokines are shown for the first time. Therefore, our data can be further used in analysis of synovial fluid chemokine profile in studies of joint disease of different etiology.