Treatment based on traditional medicine is very popular in developing world due to inexpensive properties. Nowadays, several types of preparations based on medicinal plants at different dose have been extensively recognized in the diseases prevention and treatment. In this vista, latest findings support the effect of Curcuma longa and its chief constituents curcumin in a broad range of diseases cure via modulation of physiological and biochemical process. In addition, various studies based on animal mode and clinical trials showed that curcumin does not cause any adverse complications on liver and kidney function and it is safe at high dose. This review article aims at gathering information predominantly on pharmacological activities such as anti-diabetic, anti-microbial, hepato-protective activity, anti-inflammatory, and neurodegenerative diseases.

IntroductionTumors must escape from the host's immune surveillance to survive and grow. Lymphoma is a general term for cancers that develop in the lymphatic system and it is the third most common cancer in children and adolescents. 1 To improve the outcome in patients with hematopoietic tumors, a better understanding of the immunobiology of lymphoma is essential. A novel lymphocyte population that has been identified as a key player in both innate and acquired immune responses, including as antitumor effector cells, is the natural killer T (NKT) cell. [2][3][4] NKT cells recognize lipid antigens presented by the MHC class I-like CD1d molecule and express cell surface markers shared with NK cells. 3 The vast majority of these T cells are canonical or invariant NKT (type I NKT) cells that possess a specific T-cell receptor (TCR) ␣-chain rearrangement (V␣14J␣18 in mice; V␣24J␣18 in humans), associated with V␤ chains of limited diversity. All other NKT cells that are CD1d-restricted and do not express this invariant TCR are called type II NKT cells. 5,6 Unlike type I NKT cells, little is known about type II NKT cells, but there is some evidence that type II NKT cells are a functionally important T-cell subset. 5 As CD1d molecules are vital for NKT-cell development, 7 mice lacking the CD1d1 gene (CD1KO mice) are deficient in all CD1d-restricted NKT cells (both type I and type II). 8 Mice lacking the J␣18 gene (J␣18KO mice) are deficient only in type I NKT cells. As NKT cells are capable of secreting both Th1 and Th2 cytokines, this has made it difficult to predict the consequences of their activation in vivo but has nonetheless created much speculation that they play a central role in immunoregulation. 2 NKT cells are directly cytotoxic and their activation can also result in "adjuvant effects" during antitumor immune responses by activating other cytotoxic lymphocytes, mainly through a Th1 cytokine cascade. 4 However, there are reports demonstrating a suppressive antitumor role for CD4 ϩ NKT cells in some murine tumor models, 9 and type II NKT cells were shown to be capable of down-regulating tumor immunosurveillance. 10 The role of NKT cells in the evasion of hematopoietic tumors from the host's innate antitumor immune response in vivo has only recently begun to be investigated, and we have reported that type I NKT cells play an inhibitory role in a murine T-cell lymphoma model. 11 Several human hematopoietic cell types express CD1d on their surface, 12 but the overall role of CD1d in antitumor immunity is not well understood. We have previously demonstrated that certain hematopoietic tumors shed glycolipids that mask CD1d-mediated antigen presentation to both type I and II NKT cells. 13 Recently, in vitro killing of EL-4 T-cell lymphoblastic lymphoma cells by type I NKT cells and their in vivo eradication in a CD1d-dependent manner has been reported. 14 CD11b and Gr-1 are the most common markers found on myeloid derived suppressor cells (MDSCs) and these cells are distinct from T lymphocytes and NK cells. 15 Accum...

A critical component of the host’s innate immune response involves lipid Ag presentation by CD1d molecules to NK T cells. In this study we used murine CD1d1-transfected L (L-CD1) cells to study the effect of viruses on CD1d-mediated Ag presentation to NKT cells and found that an infection with vesicular stomatitis and vaccinia (but not lymphocytic choriomeningitis) virus inhibited murine CD1d1-mediated Ag presentation. This was under the reciprocal control of the MAPKs, p38 and ERK, and was due to changes in the intracellular trafficking of CD1d1. The reciprocal regulation of CD1d1-mediated Ag presentation by MAPK suggests that the targeting of these pathways is a novel means of immune evasion by viruses.