Familial hemophagocytic lymphohistiocytosis (FHL) is

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BackgroundT-helper (Th) 22 is involved in the pathogenesis of inflammatory diseases. The roles of Th22 cells in the pathophysiological of ankylosing spondylitis (AS) and rheumatoid arthritis (RA) remain unsettled. So we examined the frequencies of Th22 cells, Th17 cells and Th1 cells in peripheral blood (PB) from patients with AS and patients with RA compared with both healthy controls as well as patients with osteoarthritis.Design and MethodsWe studied 32 AS patients, 20 RA patients, 10 OA patients and 20 healthy controls. The expression of IL-22, IL-17 and IFN-γ were examined in AS, RA, OA patients and healthy controls by flow cytometry. Plasma IL-22 and IL-17 levels were examined by enzyme-linked immunosorbent assay.ResultsTh22 cells, Th17 cells and interleukin-22 were significantly elevated in AS and RA patients compared with OA patients and healthy controls. Moreover, Th22 cells showed positive correlation with Th17 cells as well as interleukin-22 in AS and RA patients. However, positive correlation between IL-22 and Th17 cells was only found in AS patients not in RA patients. In addition, the percentages of both Th22 cells and Th17 cells correlated positively with disease activity only in RA patients not in AS patients.ConclusionsThe frequencies of both Th22 cells and Th17 cells were elevated in PB from patients with AS and patients with RA. These findings suggest that Th22 cells and Th17 cells may be implicated in the pathogenesis of AS and RA, and Th22 cells and Th17 cells may be reasonable cellular targets for therapeutic intervention.

Circular RNAs (circRNAs) represent a widespread class of non-coding RNAs, which drew little attention in the past. Recently, limited data showed their promising future to act as biomarkers in human cancer, but the characteristics and functions remain largely unknown in hematopoietic malignancies, especially in leukemia. In this study, with the help of circRNA microarray, we demonstrated the expression profile of circRNAs in acute myeloid leukemia (AML) patients, and identified a large number of circRNAs possibly expressed in a leukemia specific manner. We also described a circRNA signature related to AML risk-status based on the bioinformatics prediction. In particular, a downregulated circRNA, hsa_circ_0004277, was characterized and functionally evaluated in a cohort of 115 human samples, thus offering a potential diagnostic marker and treatment target in AML. Interestingly, we found chemotherapy could significantly restore the expression of hsa_circ_0004277, indicating the increasing level of hsa_circ_0004277 was associated with successful treatment. Furthermore, a detailed circRNA-miRNA-mRNA interaction network was presented for hsa_circ_0004277, allowing us to better understand its underlying mechanisms for function in AML.

Tumors have been known to contain a small population of cancer stem cells that initiate tumor growth and promote tumor spreading. CD133 alone or in combination with other markers is currently being used for identification and isolation of the putative cancer stem cell population from malignant tumors. CD133 is a member of the transmembrane glycoprotein family and was initially described as a surface antigen specific for human hematopoietic stem cells.(1,2) Although its biological function remains largely unknown, CD133 has been recognized as a stem cell marker for cancerous tissues. Indeed, CD133 alone or in combination with other markers is currently used for identification and isolation of the putative cancer stem cell population from malignant tumors, as well as cell lines of brain, (3,4) prostate, (5) liver, (6,7) pancreas, (8) colon (9,10) and melanoma.In a recent report, CD133 was also used to isolate cancer stem cells from lung cancer.(12) The lung cancer CD133 + subpopulation was able to grow indefinitely as tumor spheres in serum-free medium containing epidermal growth factor (EGF) and basic fibroblast growth factor (bFGF). When injected into immunocompromised mice, they readily generated xenograft tumor phenotypically identical to the tumor derived from the original unsorted cancer cells. Upon differentiation, lung cancer CD133 + cells acquired the specific lineage markers, while losing the tumorigenic potential together with the CD133 expression. (12) However, in one recent study on different in vitro phenotypes of primary glioblastomas, although most primary cells grown as tumor spheres were driven by CD133 + cells, four of the 15 cell lines grown adherently were driven by stem cell-like CD133 -tumor cells (13) and both the CD133 + and CD133 -tumor cells from these cells were similarly tumorigenic in nude mice in vivo.(13) It was also reported that both CD133 + and CD133 -metastatic colon tumor subpopulations formed colonospheres in cultures and were capable of long-term tumorigenesis in a NOD/SCID serial xenotransplantation model. (14) Furthermore, both CD133 + and CD133 -cells displayed similar frequencies of stem cell-like properties in DAOY medulloblastoma cell line.(15) Given the contradiction regarding the role of CD133 as a true cancer stem cell marker, we investigated whether the CD133 + subpopulations of a non-small cell lung cancer A549 cell line and a small lung cancer H446 cell line characteristically resemble the cancer stem cells more closely than the CD133 -subpopulations. Materials and MethodsCell culture. Human lung cancer cell lines A549 and H446 were cultured in RPMI-1640 (HyClone, Logan, UT, USA) and 10% fetal bovine serum (Tian Jin Hao Yang Biological Manufacture, Tian Jin, China) in a tissue culture incubator at 37°C under 5% CO 2 and 100% humidity. To determine the clonogenicity and regeneration ability of single cells, colony formation assay was carried out as described previously (16) with some modifications. CD133 + and CD133 -cells of A549 and H446 were resuspended in fres...

Our findings suggest that CTLs are activated in chronic ITP and might be involved in the pathogenesis of this disorder. Apoptosis and perforin/granzyme-mediated cytotoxicity constitute an important pathway through which CTLs destruct autologous platelets. CTLs might be a reasonable target for a therapeutic strategy.

Together, our results indicated a possible role of Th22 pure Th17 cells and Th17 cells in RA, and blockade of the interleukin-22 may be a reasonable therapeutic strategy for RA.

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