The results of Smyth et al. and Barcelo et al. showed opposite results – they observed an increased proportion of Tregs in the bronchoalveolar lavage fluid (BALF) of smokers with COPD when compared to control group, moreover this proportion was higher in the BALF than in blood [17, 18]. This is to be expected, as immune cells in the lung are highly activated, much more than those in the systemic circulation, and many environmental agents and coexisted lung diseases have possible influence on these cells [29]. Moreover, the differentiation of T cells to Tregs depends on local immune conditions and certain

organ tropism Ibrutinib mouse of different subpopulations of regulatory cells was observed [30]. selleck inhibitor We also investigated the expression of CTLA4 antigen on CD4+ cells. We expected the depletion

of these cells population, similarly to CD4+/CD25+ cells. However, we found a significant increase in the proportion of CTLA4+ cells and high fluorescence of CTLA4 on CD4+ cells in COPD patients. CTLA4 (CD152) is constitutively expressed on Treg cells and plays a significant role in regulation of T cell tolerance. The results of recent studies showed that there was a down regulation of CTLA4 after activation of Tregs, that CTLA4 was required for FoxP3+ cells function but played a role in the regulation of peripheral T cell tolerance in the separate pathway [16, 31, 32]. Tang et al. showed that the autoimmune disease might be exacerbated by blocking CTLA4 [31]. Wei et al. observed an elevated proportion of CTLA4 positive cells in systemic arthritis when compared with circumscribed form of the disease [27]. Recently, Zhu et al. presented that CTLA4 single nucleotide polymorphism was associated with chronic bronchitis [33]. Taken together, our findings may indicate the down regulation of CTLA4 expression concomitant with the depletion of CD4+/CD25+ cells Cell press in the blood of patients

with stable COPD. We did not find any significant correlation of proportion of CD4+/CD25+ and CTLA4+ cells with degree of airflow limitation in pulmonary function tests. This result can not be surprised when take into account that the group of patients suffered from early diagnosed stable COPD in the mild/moderate stage of the disease. The third part of this possible autoimmunological ‘jigsaw’ was adiponectin. This adipocite-derived cytokine is known to modulate the immune response and to have many anti-inflammatory effects, like: decreased production of IL-8, IL-6 and TNFα, increased production of IL-10, inhibition of macrophage foam cell development and enhancement of apoptotic cells clearance [3, 19, 20]. The increased serum levels of adiponectin in COPD patients were observed by other authors in context of body weigh loss or disease exacerbations [21, 34, 35]. The novelty of our study is that we analysed this cytokine in the context of immunity.