5 versus CHIR-99021 in vitro 38.5% in lane 5 versus lane 11 to 78.7 versus 21.3% in lane 6 versus lane 12). The densitometry data obtained from multiple blots confirmed the concomitant cytosolic accumulation of p48 and pY-STAT6 accompanied with a nuclear decrease in p48 prominent by 4 h post-IFN-α stimulation (Fig. 4B). Furthermore, co-immunoprecipitation experiments demonstrated that pY-STAT6 strongly interacts with IFN-α-induced pY-STAT2 as well as with p48 in the cytoplasm (Fig. 5A), which is also evident by 4 h after IFN-α treatment. On the other hand, neither STAT1 nor importin-α which is known to mediate

the nuclear translocation of STATs 35, interacted with pY-STAT6 (Fig. S3). By confocal analysis, the concomitant cytoplasmic accumulation of pY-STAT6 (green) and p48 (red), or that of STAT2 (green) and p48 (red) was also confirmed upon 4 h pretreatment of IFN-α followed by IL-4 stimulation (Fig. 5B). Together these data suggest that pY-STAT6 is likely to complex with IFN-α-induced pY-STAT2

and p48, and is retained in the cytosol. The concomitant cytosolic retention of pY-STAT6 by pY-STAT2:p48, and the subsequent decrease in pY-STAT6 nuclear translocation may be responsible for the inhibitory effect of IFN-α on the IL-4-activated CD23 gene expression in B cells (Fig. 1C). The above data indicate that IFN-α and IL-4 treatment induced a concurrent cytoplasmic accumulation and complex selleck screening library formation of the IFN-α-induced pY-STAT2:p48 and the IL-4-induced pY-STAT6 in Ramos B cells. As much as the resulting retention of pY-STAT6 by pY-STAT2:p48 in the cytoplasm may lead to the suppression

of IL-4 signaling into Dipeptidyl peptidase the nucleus, the retention of pY-STAT2:p48 by pY-STAT6 would have a similar role in the inhibition of nuclear localization of ISGF3 induced by IFN-α. In fact, IL-4 is shown to exert an antagonistic action on IFN-α signaling in certain cell systems 17. As an IFN-α target gene counter-regulated by IL-4 in B lymphoma cells, IRF7 was examined. As a member of IRFs involved in IFN-α response, IRF7 has been reported to be induced via IFN-α-activated ISGF3 in lymphomas and DC, and to play a role in the induction of EBV-transformed lymphoma and the activation of type I IFN genes 17, 36, 37. The quantitative RT-PCR analysis of IRF7 mRNA in Ramos B cells has revealed that IFN-α treatment induced IRF7 at a significant level by 4 to 8 h, and IL-4 reduced IFN-α-induced IRF7 mRNA levels in a time-dependent manner (Fig. 6). The result together with the data from Figs 3–5 raises a possibility that the inhibition of IL-4 on the IFN-α-induced IRF7 gene expression (Fig. 6) is probably interceded by the complex formation and cytoplasmic retention of the pY-STAT6:pY-STAT2:p48.

Besides IFN-γ, mouse dNK cells also secrete colony stimulating factor-1 (CSF-1), IL-1, leukemia inhibitory factor (LIF),55 TNF-α, and VEGF.56 Studies of human dNK cells have shown

that dNK cells produce a variety of cytokines MI-503 solubility dmso and growth factors. At the mRNA level, it was shown that human dNK cells produce transcripts of GM-CSF, CSF-1, TNF-α, LIF, and IFN-γ.57 A recent study has shown that the engagement of NKp30, but not NKp46, induces the secretion of TNF-α, MIP1-α, MIP1-β, GM-CSF, and IFN-γ by human dNK cells that were shortly activated with IL-2 or IL-15 for 48 hr.45 Human dNK cells can also secrete IL-8 and IP-10 and it was demonstrated that these chemokines bind to their receptors on invasive trophoblasts causing trophoblast migration.43 Human dNK cells can also produce a variety of angiogenic factors, including several members of the VEGF family, PLGF, angiopoetin-2 (Ang-2), and NKG5.43 These findings further support the function of dNK cells as major regulators

Staurosporine of vascular remodeling during the early stage of pregnancy. The ability of dNK cells to secrete a variety of cytokines that support these developmental processes during pregnancy suggests that dNK cells must be activated in the tissue, rather than inhibited, to exert their constructive roles at the fetal-maternal interface and establish a normal pregnancy. Indeed, it has been shown that dNK clones expressing the activating receptor KIR2DS4 generated higher amounts of IL-8, IP-10, VEGF, and PLGF than clones expressing inhibitory receptors, such as KIR2DL1. This suggests that activation of dNK cells reduces the risk of pre-eclampsia, through the production of sufficient amounts of

growth factors and chemokines by dNK cells.43 These factors contribute to trophoblast invasion and vascular modifications, as discussed above. The study of Moffet’s group strongly supports this notion as well. Their study suggested that strong inhibition of dNK cells, as a result of interactions between certain KIR alleles on dNK cells and certain HLA-C allels on extravillous trophoblasts, increases the likelihood of pre-eclampsia. Furthermore, interactions Urocanase between KIRs and HLA-C, which induce activation of dNK cells, result in a better trophoblast invasion.58 The unique properties of dNK cells probably result from intense communication between these cells and their neighboring decidual cells, local cytokines, other immune cells, and secreted hormones that create the special microenvironment of this tissue. dNK cells are in close contact with invasive trophoblasts and local decidual cells49 and therefore, there is probably a constant exposure of dNK receptors to their ligands. Indeed, decidual stromal cells express unknown ligands for the dNK-activating receptors NKp30 and NKp44.43 In addition, purified HLA-G+ trophoblasts express unknown ligands for NKp44.

Today, epidemiology has moved beyond the study of infections alone and has contributed to the link between rubber workers and bladder cancer [5], asbestos exposure and mesothelioma [62], ultraviolet radiation and skin cancer [41], and most notably, from the British Doctors study, tobacco in the etiology of lung cancer [17]. Epidemiology

is defined as the study of distribution and determinants of health-related Vemurafenib cost states and the use of such studies to address health-related problems. The main aim of the science is to discover potential causal relationships, which may be further tested with appropriate modifications to remove the possible trigger and assess the potential benefits. In 1965, Austin Bradford Hill detailed criteria for assessing evidence of causation (Table 1) [25]. It is important to stress that these are nothing more than a series of tests to apply to a hypothesis to determine its relative strength; they do not form a checklist that if all criteria are met, causality is proven. At this point, it is important to distinguish between true epidemiological studies and population-based mechanistic studies. Epidemiological studies are primarily designed to reveal relationships between exposures to substances,

such as alcohol Selleckchem Palbociclib and smoking, to outcomes, such as cardiovascular events or death. This contrasts with the larger population-based studies that are aimed at determining and measuring physiological or pathological processes, and exploring their relationships with morbidity, mortality, or surrogates thereof. The

utility of large populations PAK5 and statistical methods established in epidemiology often results in these microvascular mechanistic studies being referred to as “epidemiological.” These large-scale studies have considerable overlap with epidemiology, notably in the application of the Bradford-Hill criteria of causation, study designs (Table 2), and statistical modeling to account for other known mechanistic processes and potential confounding, however, have the important distinction that these are exploring relationships between structure and/or function within one microvascular beds and outcomes, without looking directly at the impact of external influences. Cardiovascular disease, encompassing, but not limited to, atherosclerotic coronary artery disease, stroke, peripheral vascular disease, and hypertensive target organ damage, is the biggest cause of premature death and disability in the developed world [74], and much work has been performed to better understand its etiology. Despite this, much of the variance in these disease processes remains unexplained [75]. Furthermore, the exact mechanisms associating, for example, hypertension and atherosclerosis are unclear. A greater understanding of these etiopathogenic mechanisms may allow further drug development or nonpharmacological interventions to be applied to populations.

Furthermore, mouse analogues of these co-stimulatory-attenuated tolDC have been shown to prevent diabetes onset in non-obese diabetic (NOD) mice [79]. Ten million control DC or tolDC were injected intradermally into find protocol the abdominal wall once every 2 weeks for a total of four administrations, and patients were monitored subsequently for a period of 12 months. DC treatment was well tolerated without any adverse events. DC treatment did not increase or induce autoantibodies (e.g. insulinoma-associated protein-2 antibodies). Furthermore, despite the fact that serum levels of IL-10 and IL-4 were increased, patients did not

lose their capability to mount T cell responses to CT99021 supplier viral peptides or allogeneic cells, indicating that DC treatment did not result in systemic immunosuppression. The percentages of immune cell subsets in peripheral blood did not change after DC treatment, with the notable exception of B220+/CD11c– B cells. The proportions of this subset were increased significantly after DC treatment, although their levels returned to baseline after 6 months of treatment. This subset of B cells displayed suppressive activity in vitro and their proportional enhancement may be a beneficial effect

of DC treatment. Overall, there were no notable differences between treatment with control DC and tolDC. Control DC were immature and therefore in a tolerogenic state; thus, it is not surprising that both types of DC exerted similar, potentially

‘pro-tolerogenic’ effects, i.e. enhancing IL-4 and IL-10 and the proportion of regulatory B cells. However, as it cannot be excluded that immature DC may become immunogenic DC in vivo, treatment Thymidylate synthase with stable tolDC remains the preferred option. A Phase I study with autologous tolDC in patients with RA has been carried out by Ranjeny Thomas and colleagues at the University of Queensland. Preliminary data were reported at the European League against Rheumatism meeting (EULAR) in 2011 [77]. In this study tolDC were generated by treatment of monocyte-derived DC with an inhibitor of NFκB signalling, BAY 11–7082, shown previously to maintain mouse DC in a tolerogenic state by preventing DC maturation [54, 80]. BAY-treated tolDC are deficient for CD40 expression but express high levels of CD86 [80, 81]; thus, they are phenotypically different from the co-stimulation-attenuated tolDC developed by the Giannoukakis/Trucco team [79]. Furthermore, unlike the trial in type I diabetes, in which tolDC were not loaded with a relevant autoantigen, in this trial tolDC were pulsed with four citrullinated peptide antigens. The final, antigen-pulsed, tolDC product is referred to as ‘Rheumavax’.

DNA and RNA are then detected by, respectively, TLR7 and TLR9 and trigger MyD88- and IRF1-dependent responses. Interestingly, our data indicating that actin polymerization and phagocytosis are not required for dectin-1-dependent cytokine induction (e.g. for S. cerevisiae-induced TNF-α secretion) are in agreement with a recent report showing that dectin-1 can be activated by β-glucan immobilized on a nonphagocytosable surface (such as a culture plate), occurs prior to initiation of phagocytic cup formation and BEZ235 ic50 is not dependent on actin dynamics [55]. Altogether our data, pointing to the importance in anti-fungal defenses of the latter pathway, may be useful to better

understand the strategies used by C. albicans to evade the innate immune system and to devise alternative Alvelestat nmr therapeutic strategies. Knock-out mice were originally obtained from T. Taniguchi (IRF1−/−, IRF3−/−, and IRF7−/−), and S. Akira (TLR2−/−, TL3−/−, TLR4−/−, TLR7−/−, TLR9−/−, MyD88−/−, Mal−/−, TRAM−/−

and TRIF−/−) as previously described [29]. Dectin 1−/−, 3d and TLR7/9 double Ko (TLR7−/−/TLR9−/−) mice were provided by, respectively, G. Brown [11], B. Beutler [35] and S. Bauer. C57BL/6 WT mice, used as controls, were purchased from Charles River Laboratories (Calco, Italy). The mice were housed and bred under pathogen-free conditions in the animal facilities of the Elie Metchnikoff Department, University of Messina. All studies were performed in agreement with the European Union guidelines of animal care and were approved by the Ethics Committee of the Metchnikoff Department of the University of Messina (CESA) and by the relevant national authority (Istituto Superiore di Sanità). C. albicans (ATCC 90028) was purchased from the American Type Culture Collection. S. cerevisiae strain A11 was isolated in the clinical mycology

laboratory of the Elie Metchnikoff Department, University Rho of Messina [22]. For in vivo and in vitro experiments, these two strains were grown in a chemically defined medium as previously described [22]. CFU numbers used in each experiment were determined after plating on Sabouraud dextrose agar (Difco Laboratories). Heat killed C. albicans strains were prepared as previously described [22], followed by washing with PBS and resuspension to the original volume. Depleted zymosan (i.e. hot alkali-treated zymosan, which is devoid of TLR-dependent stimulating properties) and control stimuli (poly I:C, Escherichia coli ultrapure LPS, CpG B, CL264) were purchased from InvivoGen. Curdlan was purchased from Wako Pure Chemicals and detoxified using cold NaOH treatment [22]. Fungal cell extracts were obtained by vortexing of C. albicans (grown in the mid-log phase) in the presence of glass beads 425–600 μm in diameter (Sigma).

The aim of this study is to evaluate the association of the course of depression symptoms, based on repeated assessments of depression symptoms over time, with left

ventricular mass index (LVMI) and left ventricular filling pressure (LVFP) in patients on haemodialysis (HD). Methods:  The level of depression symptoms in 61 patients on HD were prospectively assessed using the Beck Depression Inventory (BDI) at baseline and at three intervals (5, 10, 15 months). Doppler echocardiographic examinations were performed at the end of follow up. Results:  At the end of follow up, the patients were divided into three groups according to their course of depression symptoms: non-depression Cabozantinib (n = 21), intermittent depression (n = 23) and persistent depression (n = 17). LVMI and LVFP were significantly increased in the persistent depression symptoms group compared to those of the non-depression symptoms group and the intermittent depression symptoms group. Persistent depression symptoms were independently associated with LVMI (β-coefficient = 0.347, P = 0.017)

and LVFP (β-coefficient = 0.274, P = 0.048) after adjustment for age, sex, systolic blood pressure, diastolic blood pressure, diabetes and interdialytic weight gain. Conclusion:  In our study, persistent depression symptoms were associated with left ventricular hypertrophy and diastolic dysfunction. Our data may provide a more complete understanding of cardiovascular risk associated with depression symptoms in patients buy Sirolimus on HD. “
“Aim:  The role of the tumour necrosis factor-like weak inducer of apoptosis (TWEAK)/Fn14 and interferon-inducible protein (IP-10)/CXCR3 axis in the pathogenesis of lupus nephritis were studied. Methods:  The mRNA expression of TWEAK, Fn14, IP-10 and CXCR3 were quantified in the glomerulus and tubulointerstitium of 42 patients with lupus nephritis (LN group) and 10 healthy controls.

Results:  As compared to controls, LN patients had higher glomerular expression of TWEAK and Fn14, but glomerular CXCR3 expression was lower in the LN group. Similarly, the LN group had higher tubulointerstitial expression of TWEAK and Fn14, but lower tubulointerstitial expression of CXCR3, than controls. Glomerular TWEAK expression DOK2 of class V nephritis was significantly higher than class IV nephritis. Glomerular expression of CXCR3 significantly correlated with proteinuria (r = −0.532; P = 0.019), whereas tubulointerstitial CXCR3 significantly correlated with serum creatinine (r = −0.447; P = 0.029). Conclusion:  In patients with lupus nephritis, there is an increase in intra-renal expression of TWEAK and Fn14, and a decrease in CXCR3 expression. Intra-renal expression of CXCR3 correlates with proteinuria and renal function. Our findings suggest that the TWEAK/Fn14 and IP-10/CXCR3 axis may contribute to the pathogenesis of lupus nephritis.

The number of isolates of various viruses detected in public health laboratories all over Japan is available in the Infectious Agents Surveillance Report, Japan, for each year since 1981, the data between 1980 and 1991 being documented in published supplements (7, 8). All annual data are available from the NESID system (14). This NESID system database includes the data from Yamagata described in this study.

Several previous studies have reported that HPIV1 infections have clear outbreaks in autumn, mostly in September and November, either every two years (15–18) Doxorubicin molecular weight or at irregular intervals (19). In this study, we found no clear seasonality for HPIV1 infections, although HPIV1 infections did appear to be more common in odd-numbered years. In Japan, no source, including the NESID system, has indicated a seasonal pattern in HPIV1 infections (5–8, 14). In comparison to the clear seasonality of HPIV1 and HPIV3 outbreaks, smaller yearly or irregular outbreaks of HPIV2

have reportedly occurred in autumn (15–19). In this study, we recovered many HPIV2 isolates in the autumn-winter season, observing a particular increase in even-numbered years since 2004 in Yamagata, Japan. The NESID system data support this trend: in the years prior to 1986, HPIV2 infections occurred more commonly in even-numbered years, apart from 1981 and 1983 selleck chemicals (7, 8, 14). Thus, HPIV2 infections have commonly occurred in the autumn-winter season every two years in Japan, although this seasonality is less clearly observable than that of HPIV3. In this study from 2002 to 2011 in Yamagata, Thalidomide Japan, we found HPIV3 infections to be grouped in clear

yearly seasonal outbreaks, mainly between May and July. The data in the NESID system also show that HPIV3 infections have peaked in the spring-summer season since 1980 (7, 8, 14). Many previous studies have reported that HPIV3 causes yearly outbreaks, mainly in the spring-summer season, around the globe (15–20); the clear seasonality of HPIV3 in Yamagata appears similar to that observed in other areas. It is generally accepted that HPIV3 as well as RSV infections are common in infants and young children, whereas HPIV1 and HPIV2 infections tend to be commoner in older persons (1–3, 15, 19). Knott et al. reported that the age distribution of HPIV3 infections peaks at 6 months–2 years of age, whereas HPIV1 and HPIV2 peak at 2–5 years (15): findings that are similar to our observations in this study. Clinically, fewer of our patients were diagnosed with croup (2.3–8.2%) than was reported by Knott et al. (9–45%) (15). However, both studies supported the contention that HPIV1 and HPIV2 are more strongly associated with croup than is HPIV3, which is in agreement with the trends described in various textbooks (1, 3). This study indicates that the annual isolation frequencies of HPIV1–3 are 1.6–10.

In addition to their involvement of mast cells in anaphylaxis, atopic asthma and other allergic disorders, mast cells are increasingly being recognized as regulators of innate or adaptive immune responses. Stephen Roscovitine mw J. Galli (Stanford, CA) proposed three hypotheses that: the potential to perform negative, as well as positive, immunomodulatory functions

is a basic property of the mast cell lineage; the mast cells can enhance and/or later help to limit certain innate and acquired immune responses and the extent to which mast cells actually perform such positive or negative immunomodulatory functions during specific immune responses in vivo is highly dependent on the individual biological setting. He also described mouse models used to analyse mast cell function in LEE011 solubility dmso vivo and to identify potential immunomodulatory roles for mast cells during specific immune responses

27. He observed that mast cell proteases can diminish the toxicity and mortality associated with either high concentrations of endogenous peptides (e.g. endothelin-1 or neurotensin) or exposure to the venom of certain poisonous snakes or the honey bee. In these settings, mast cells can limit morbidity and death at least in part by providing proteases that degrade the endogenous peptides or components of the venom within the skin. In addition, evidence derived from studies in mast Selleckchem Ponatinib cell-engrafted WBB6F1-KitW/W-v or C57BL/6-KitW-sh/W-sh genetically mast cell-deficient mice indicates that mast cells can limit the magnitude and/or promote the resolution of certain innate or adaptive immune

responses by producing IL-10 and other products which can mediate a potentially wide variety of anti-inflammatory or immunosuppressive effects 28. Dr. Galli recommended, when it is feasible (and it sometimes is not), using both types of mast cell-engrafted mice (i.e. employing WBB6F1-KitW/W-v and C57BL/6-KitW-sh/W-sh mice as recipients of the corresponding WT or genetically altered mast cells) to investigate roles of mast cells in vivo. He also recommended the development and careful evaluation of additional models, including putative “mast cell-specific Cre mice”, in order to expand the array of tools available to study the roles of mast cells and their products in vivo. However, he emphasized that it is important that results obtained with each of the established or newer models be interpreted with thoughtful consideration of both the advantages and any potential limitations of the models used. Stephanie Eisenbarth (New Haven, CT) described the role of inflammasomes in adjuvants and allergic disease. Aluminum adjuvants, typically referred to as “alum”, are the most commonly used adjuvants in human and animal vaccines worldwide; yet, the mechanism underlying alum’s stimulation of the immune system has only recently been elucidated.

All of these 10 patients had nephrotic syndrome on presentation (p = 0.008) and their serum creatinine level a month after renal biopsy elevated significantly (p = 0.003). Survival rate was significantly worse in the patients with gastrointestinal

(GI) involvement (p = 0.01) on presentation. During the observation dialysis was introduced in 7 patients. Three patients were successfully withdrawn from dialysis within a month buy KU-57788 and 4 patients required maintenance dialysis. Renal survival were significantly worse in the patients with nephrotic syndrome or GI involvement (p = 0.0002 or p = 0.0003, respectively). International Study of Kidney Disease in Children (ISKDC) grade was more than III in all of the patients who Erlotinib molecular weight required dialysis. Furthermore, factors

affecting renal survival were as follows: rate of crescentic glomeruli in renal biopsy findings, serum creatinine and daily urinary protein at the time of renal biopsy, maximum serum creatinine level and daily urinary protein during observation period. In immunofluorescence microscopy glomerular IgG deposition did not contribute to the renal or survival outcome. Conclusion: Nephrotic syndrome and GI involvement predict worse renal and survival outcome in our retrospective cohort of IgA vasculitis. Crescent formation, serum creatinine and dairy urinary protein have prognostic value for renal outcome. JAMBA ARIUNBOLD1, KONDO SHUJI1, URUSHIHARA MAKI1, NAGAI TAKASHI1, KIM-KANEYAMA JOO-RI2, MIYAZAKI AKIRA2, KAGAMI SHOJI1 1Department of Pediatrics, Institute

of Health Bioscience, The University of Tokushima Graduate School; 2Department of Biochemistry, Showa University School of Medicine Introduction: Hydrogen peroxide-inducible clone-5 (Hic-5) is a transforming growth factor (TGF)-β1-inducible focal adhesion protein. We recently demonstrated that Hic-5 was localized in mesangial cells (MC) and its expression has http://www.selleck.co.jp/products/Abiraterone.html been associated with glomerular cell proliferation and matrix accumulation in rat and human glomerulonephritis (GN) (Nephron Exp Nephrol 120: e59–68, 2012). However, how Hic-5 is involved in the development of GN remains to be determined. Methods: We assessed the role of Hic-5 in mesangial proliferative GN in wild type (Hic-5+/+) and Hic-5 deficient (Hic-5-/-) mice. Mesangial proliferative GN was induced by intravenous injection of Habu venom (4 mg/kg) 7 days after removing a right kidney. Samples were obtained at sacrifice day 7. Glomerular cell number and matrix score analysis are examined and followed by immunohistochemical analysis for expression of matrix proteins and α-smooth muscle actin (SMA). To clarify the effect of Hic-5 about MC proliferation, we developed and characterized cultured MC though magnetic based-isolation of glomeruli from Hic-5+/+ and Hic-5−/− mice.

8%

versus 216.6, P = 0.048. CD25high cells formed about 7% of CD4+/CD25+ cells and the proportion differed significantly NVP-BEZ235 order between investigated groups being lower in the patients than in controls (5.2% versus 7.5%, P = 0.03). The proportion of CTLA4+ cells as a percentage of CD25+ cells was significantly higher in the patients when compared with healthy persons (10.4% versus 4.7%, P = 0.014) (Fig. 2c). The mean fluorescence of CTLA4 on lymphocytes in patients was 189% and was higher than in healthy subjects 150%, difference not significant. There were no differences in the lymphocyte subtypes between smokers and nonsmokers in the group of patients and of controls, as well. The proportion of T-cell subpopulations did not differ between smokers and ex-smokers in patients XL765 datasheet with COPD. There was an inverse relation of the proportion of T-helper cells with smoking history expressed as pack years smoked (R = –0.55, P < 0.05) in the COPD group. The mean serum concentration of adiponectin was 15.4 ± 13.3 μg/ml in COPD patients and 8.5 ± 7.58 μg/ml in controls (P = 0.021) (Fig. 3). The mean adiponectin to body mass index (BMI) ratio was

0.38 ± 0.27 in patients versus 0.28 ± 0.14 in controls, difference not significant. The proportion of CD3+ cells correlated with disease duration (R = 0.7, P < 0.05). There was a significant correlation of the proportion of CTLA4+ cells with the proportion of CD8+/CD25+ (R = 0.62, P < 0.05). We did not find no more relevant correlations of proportion of cell subtypes with

demographic data. Especially no correlation of the proportion of lymphocyte subtypes with the age of investigated persons was observed. The mean age in the patients group was slightly higher than in the control group. However, after grouping Resminostat investigated persons into the groups in comparable age, the differences in the proportion of cells noted above remained significant. No significant correlations of results of pulmonary function tests with proportion of cell subpopulations were found. We observed significant negative correlation of adiponectin concentration with BMI in the group of patients (R = –0.85, P < 0.05). The adiponectin/BMI ratio correlated with the decrease of FEV1% and with decrease of FEV1%FVC (R = –0.59, P < 0.05). The adiponectin/ BMI ratio correlated with proportion of T-helper cells (R = 0.6, P < 0.05). The systemic inflammation in the course of COPD is a fact but its aetiology and pathogenesis remain unclear and are recently widely investigated [2]. In this study, we presented one fragment of the complicated inflammatory pathways: some elements that are known to be active in autoregulation of the immune response. We found significant alterations in the population of T lymphocytes with regulatory properties in patients with mild/moderate COPD.