Showing posts with label lupus. Show all posts
Showing posts with label lupus. Show all posts

Friday, June 25, 2010

The imbalance between regulatory and IL-17-secreting CD4+ T cells in lupus patients

"The present study indicates that active SLE appears to exist as an imbalance between Treg and Th17 cells. Correction of this Treg/Th17 imbalance may have therapeutic impact for patients with SLE."


Link: CiteULike: The imbalance between regulatory and IL-17-secreting CD4+ T cells in lupus patients:

Thursday, June 24, 2010

Oxidative and nitrosative stress contribute to lupus disease activity

University of Texas Medical Branch researchers have uncovered an association between free radical-mediated reactions and the severity and progression of system lupus erythematosus (SLE). Higher levels of oxidative and nitrosative stress markers were found in SLE patients with greater disease activity suggesting a causal relationship. Full findings of the study are available in the July issue of Arthritis & Rheumatism, a journal published by Wiley-Blackwell on behalf of the American College of Rheumatology.


Oxidative and nitrosative stress contribute to lupus disease activity:

Thursday, March 25, 2010

Dysregulated immune balance in lupus.

Our data indicate that the mechanisms involved in balancing Th1 and Th17 regulation, as well as in producing IL-6, are aberrant in SLE, leading to an increased Th17 response.
CiteULike: Dysregulated balance of Th17 and Th1 cells in systemic lupus erythematosus: "Shah, K., Lee, W. W., Lee, S. H., Kim, S. H., Kang, S. W., Craft, J., and Kang, I. (2010). Dysregulated balance of th17 and th1 cells in systemic lupus erythematosus. Arthritis Research & Therapy, 12(2):R53+."

Tuesday, November 3, 2009

Promise Of A New Lupus Treatment Is A Groundbreaking Achievement

Human Genome Sciences (HGS) and GlaxoSmithKline (GSK) today announced positive results from BLISS-76, the second of two large-scale phase III clinical trials of BENLYSTA™ (belimumab) for treating systemic lupus. A full presentation of results from BLISS-52 was recently shared at the 73rd Annual Scientific meeting of the American College of Rheumatology.. Click here.

Monday, October 26, 2009

Genetic dissection of systemic autoimmune disease in nrf2 deficient mice.

Title: Genetic dissection of systemic autoimmune disease in nrf2 deficient mice.

Summary: "SLE occurs with an prevalence as high as 1 in 2,500 people but predominantly affects women (35). SLE is especially prevalent in women during their childbearing years (9:1 female to male ratio) and during pregnancy, suggesting a role of female hormones in development of the disease. Most mouse models of SLE also exhibit an increased susceptibility of females to the disease. The sex-specific decreases in glutathione S-transferase -1 and -2 and ยต-1, -2, and -3 have been shown previously in the livers of nrf2 knockout mice (10) and are in agreement with our study (Table 3). The findings from this data and other reports strongly suggest that a deficiency in detoxification and increased oxidative stress can result in the development of a systemic autoimmune disease."

Li, J., Stein, T. D., and Johnson, J. A. (2004). Genetic dissection of systemic autoimmune disease in nrf2 deficient mice. Physiological Genomics, pages 1-57.  http://www.citeulike.org/user/HEIRS/article/6012655

Sunday, October 18, 2009

New study identifies cellular mechanism that causes lupuslike symptoms in mice

New study identifies cellular mechanism that causes lupuslike symptoms in mice

Macrophages, the scavenger cells of the body's immune system, are responsible for disposing of dying cells. Stanford University School of Medicine researchers have identified one pathway in this important process in mice that, if disrupted, causes a lupuslike autoimmune disease.