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The most recently recognized types of immune cells, the innate lymphoid cells (ILCs), have been sub-divided according to respective distinct expression profiles of regulatory factors or/and cytokines. ILCs have also been shown to participate in a variety of beneficial immune responses, including participation in attack against pathogens and mediation of the pre-inflammatory and inflammatory responses through their production of pro-inflammatory cytokines. As such, while the ILCs exert protective effects they may also become detrimental upon dysregulation. Indeed, recent studies of the ILCs have revealed a strong association with the advent and pathogenesis of several common autoimmune diseases, including psoriasis, inflammatory bowel disease (IBD) and multiple sclerosis (MS). Though the ILCs belong to lineage negative cells that are distinctive from the Th cells, the profiles of secreted cytokines from the ILCs overlap with those of the corresponding Th subsets. Nevertheless, considering that the ILCs belong to the innate immune system and the Th cells belong to the adaptive immune system, it is expected that the ILCs should function at the early stage of diseases and the Th cells should exert predominant effects at the late stage of diseases. Therefore, it is intriguing to consider targeting of ILCs for therapy by targeting the corresponding cytokines at the early stage of diseases, with the late stage cytokine targeting mainly influencing the Th cells' function. Here, we review the knowledge to date on the roles of ILCs in various autoimmune diseases and discuss their potential as new therapeutic targets. [ABSTRACT FROM AUTHOR]

It has been reported that sphingosine kinase 1 (SPHK1), an oncogenic enzyme, was involved in the development and progression of a number of human cancers. However, the role of SPHK1 in nasopharyngeal carcinoma (NPC) is largely unknown. The present study aimed to characterize the expression of SPHK1 in human NPC and evaluate its clinical significance. Real-time quantitative reverse transcriptase–polymerase chain reaction (qRT-PCR) and Western blot analyses showed that the expression of SPHK1 mRNA and protein in NPC specimens was significantly higher than that in non-tumorous nasopharyngeal mucosa biopsies. Immunohistochemistry (IHC) was conducted to characterize the expression pattern of SPHK1 in 142 archived paraffin-embedded NPC specimens. Statistical analyses revealed that high levels of SPHK1 expression were associated with the clinical stages, locoregional recurrence and distant metastasis of NPC. NPC patients with high levels of SPHK1 expression had shorter survival time, whereas those with lower levels of SPHK1 expression survived longer. Moreover, multivariate analysis suggested that SPHK1 up-regulation was an independent prognostic factor for NPC. Our results suggest for the first time that SPHK1 is involved in the development and progression of NPC, which can be used as a useful prognostic marker for NPC patients and may be an effective target for treating NPC. [ABSTRACT FROM AUTHOR]

Abstract: Increased lymphocyte apoptosis has been suggested to contribute to the development of systemic lupus erythematosus (SLE), but the critical factors involved in the apoptotic pathways are still unknown. By long serial analysis of gene expression (LongSAGE) profiles and microarray analyses, a novel apoptosis-related gene BclGL expression was found significantly increased in peripheral blood CD4+ T cells of SLE patients, which was correlated with the enhanced CD4+ T cells apoptosis, anti-nuclear antibody (ANA) titer and proteinuria. In vitro, BclGL expression could be specially upregulated by SLE serum stimulation and positively correlated with induced CD4+ T cell apoptosis. Enforcing BclGL overexpression by lentivirus could directly enhance CD4+ T cell apoptosis, but these apoptosis-inducing effects could be partially inhibited by knockdown of BclGL expression. Collectively, these results indicate that increased BclGL expression may contribute to the aberrant CD4+ T cell apoptosis which causes an inappropriate immune response and impaired homeostasis in SLE. [Copyright &y& Elsevier]