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Query: UMLS:C0024141 (
systemic lupus erythematosus
)
44,322
document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)
Systemic lupus erythematosus
(
SLE
) is an autoimmune disease characterized by several immunological abnormalities. The pathogenic importance of T cells in this disease is well established.
Interleukin-16
(
IL-16
) is a cytokine which is mainly produced by CD8+ T cells and induces chemotaxis of CD4+ T cells and monocytes.
IL-16
levels have been shown to be elevated in
SLE
patients in a cross-sectional study, but the mechanism is unknown. To explore whether the increased
IL-16
levels are associated with genetic background or the disease itself, we investigated the
IL-16
level in healthy first-degree family members of
SLE
patients and
SLE
patients who were followed over time with regard to disease activity. We observed high
IL-16
levels in
SLE
patients with severe disease compared to
SLE
patients with non-severe disease and healthy controls. Furthermore,
IL-16
levels in first-degree relatives were not different from those in healthy controls. These results suggest that high
IL-16
levels are associated with severity of
SLE
, but not with genetic susceptibility to
SLE
. Finally, we followed the disease activity of
SLE
patients over time, which showed significant correlation between the
SLE
disease activity index and
IL-16
, ESR and the complement components C3, C4 and CH50. In conclusion, these results implicate an association of
IL-16
with
SLE
.
Lupus
2002
PMID:Elevated IL-16 levels in patients with systemic lupus erythematosus are associated with disease severity but not with genetic susceptibility to lupus. 1199 83
Over the past two decades, our understanding of
interleukin-16
(
IL-16
) has increased substantially. Initial studies characterizing
IL-16
as a chemotactic cytokine (but not a chemokine) just scratched the surface of the unique properties of this cytokine. Since then, scientists have determined that
IL-16
has a wide range of effects on cells, including upregulation of CD25, induction of cells to progress to the G(1) phase, inhibition of antigen- specific proliferation yet with retained antigen nonspecific proliferative properties, and discovery of a novel neuronal form with unique properties. Recently, a plethora of studies have implicated
IL-16
in exacerbation of infectious, immune-mediated, and autoimmune inflammatory disorders, including atopic dermatitis, irritable bowel syndrome,
systemic lupus erythematosus
, neurodegenerative disorders, and viral infections. Herein, we review the body of evidence supporting a role for
IL-16
in infectious and immune-mediated inflammatory disorders and explore the known and possible mechanism of actions in the numerous diseases.
...
PMID:Not-so-sweet sixteen: the role of IL-16 in infectious and immune-mediated inflammatory diseases. 1688 62
The role of natural killer (NK) T cells in the development of
lupus
-like disease in mice is still controversial. We treated NZB/W mice with anti-NK1.1 monoclonal antibodies (mAbs) and our results revealed that administration of either an irrelevant immunoglobulin G2a (IgG2a) mAb or an IgG2a anti-NK1.1 mAb increased the production of anti-dsDNA antibodies in young NZB/W mice. However, the continuous administration of an anti-NK1.1 mAb protected aged NZB/W mice from glomerular injury, leading to prolonged survival and stabilization of the proteinuria. Conversely, the administration of the control IgG2a mAb led to an aggravation of the
lupus
-like disease. Augmented titres of anti-dsDNA in NZB/W mice, upon IgG2a administration, correlated with the production of BAFF/BLyS by dendritic, B and T cells. Treatment with an anti-NK1.1 mAb reduced the levels of
interleukin-16
, produced by T cells, in spleen cell culture supernatants from aged NZB/W. Adoptive transfer of NK T cells from aged to young NZB/W accelerated the production of anti-dsDNA in recipient NZB/W mice, suggesting that NK T cells from aged NZB/W are endowed with a B-cell helper activity. In vitro studies, using purified NK T cells from aged NZB/W, showed that these cells provided helper B-cell activity for the production of anti-dsDNA. We concluded that NK T cells are involved in the progression of
lupus
-like disease in mature NZB/W mice and that immunoglobulin of the IgG2a isotype has an enhancing effect on antibody synthesis due to the induction of BAFF/BLyS, and therefore have a deleterious effect in the NZB/W mouse physiology.
...
PMID:Long-term administration of IgG2a anti-NK1.1 monoclonal antibody ameliorates lupus-like disease in NZB/W mice in spite of an early worsening induced by an IgG2a-dependent BAFF/BLyS production. 1839 73
In our earlier study, we utilized a Bayesian design to probe the association of approximately 1000 genes (approximately 10,000 single-nucleotide polymorphisms (SNPs)) with
systemic lupus erythematosus
(
SLE
) on a moderate number of trios of parents and children with
SLE
. Two genes associated with
SLE
, with a multitest-corrected false discovery rate (FDR) of <0.05, were identified, and a number of noteworthy genes with FDR of <0.8 were also found, pointing out a future direction for the study. In this report, using a large population of controls and adult- or childhood-onset
SLE
cases, we have extended the earlier investigation to explore the
SLE
association of 10 of these noteworthy genes (109 SNPs). We have found that seven of these genes exhibit a significant (FDR<0.05) association with
SLE
, both confirming some genes that have earlier been found to be associated with
SLE
(PTPN22 and IRF5) and presenting novel findings of genes (KLRG1,
interleukin-16
, protein tyrosine phosphatase receptor type T, toll-like receptor (TLR)8 and CASP10), which have not been reported earlier. The results signify that the two-step candidate pathway design is an efficient way to study the genetic foundations of complex diseases. Furthermore, the novel genes identified in this study point to new directions in both the diagnosis and the eventual treatment of this debilitating disease.
...
PMID:Identification of new SLE-associated genes with a two-step Bayesian study design. 1944 Feb