CS - your reccomendations for lupus / Autoimmunity

Ligands to Nucleic Acid–Specific Toll-Like Receptors and the Onset of Lupus Nephritis
Rahul D. Pawar, Prashant S. Patole, Andreas Ellwart, Maciej Lech, Stephan Segerer, Detlef Schlondorff and Hans-Joachim Anders
Medical Policlinic, University of Munich, Munich, Germany

Address correspondence to: Dr. Hans-Joachim Anders, Medizinische Poliklinik, Klinikum der Universität–Innenstadt, Pettenkoferstrasse 8a, 80336 Munich, Germany. Phone: +49-89-218075846; Fax: +49-89-218075860; E-mail: hjanders@med.uni-muenchen.de

Received for publication March 23, 2006. Accepted for publication September 19, 2006.

Abstract

Lupus nephritis develops from a combination of genetic and environmental factors such as microbial infection. A role for microbial nucleic acids (e.g., via nucleic acid–specific Toll-like receptors [TLR]) was hypothesized, in this context, because microbial nucleic acids can trigger multiple aspects of autoimmunity in vitro and in vivo. Eight-week-old MRLlpr/lpr and MRL wild-type mice received an injection of pI:C RNA (ligand to TLR-3), imiquimod (ligand to TLR-7), or CpG-DNA (ligand to TLR-9) on alternate days for 2 wk. Only CpG-DNA triggered the onset of lupus nephritis in MRLlpr/lpr mice, as defined by diffuse proliferative glomerulonephritis associated with glomerular IgG and complement C3 deposition, proteinuria, and glomerular macrophage infiltrates. None of the compounds caused DNA autoantibody production or glomerulonephritis in MRL wild-type mice. The role of CpG-DNA to trigger lupus nephritis in MRLlpr/lpr mice was found to relate to its potent immunostimulatory effects at multiple levels: B cell IL12p40 production, B cell proliferation, double-stranded DNA autoantibody secretion, and dendritic cell IFN-α production. The induction of lupus nephritis by CpG-DNA is motif specific and could be prevented by co-injection of inhibitory DNA. In summary, among the ligands tested, CpG-DNA triggers lupus nephritis in genetically predisposed hosts. These data support the concept that systemic lupus erythematosus is triggered by pathogens that release CG-rich DNA.
Introd

aWell aware of some of the underlying causes, but what can I do short term?

Ligands to Nucleic Acid–Specific Toll-Like Receptors and the Onset of Lupus Nephritis
Rahul D. Pawar, Prashant S. Patole, Andreas Ellwart, Maciej Lech, Stephan Segerer, Detlef Schlondorff and Hans-Joachim Anders
Medical Policlinic, University of Munich, Munich, Germany

Address correspondence to: Dr. Hans-Joachim Anders, Medizinische Poliklinik, Klinikum der Universität–Innenstadt, Pettenkoferstrasse 8a, 80336 Munich, Germany. Phone: +49-89-218075846; Fax: +49-89-218075860; E-mail: hjanders@med.uni-muenchen.de

Received for publication March 23, 2006. Accepted for publication September 19, 2006.

Abstract

Lupus nephritis develops from a combination of genetic and environmental factors such as microbial infection. A role for microbial nucleic acids (e.g., via nucleic acid–specific Toll-like receptors [TLR]) was hypothesized, in this context, because microbial nucleic acids can trigger multiple aspects of autoimmunity in vitro and in vivo. Eight-week-old MRLlpr/lpr and MRL wild-type mice received an injection of pI:C RNA (ligand to TLR-3), imiquimod (ligand to TLR-7), or CpG-DNA (ligand to TLR-9) on alternate days for 2 wk. Only CpG-DNA triggered the onset of lupus nephritis in MRLlpr/lpr mice, as defined by diffuse proliferative glomerulonephritis associated with glomerular IgG and complement C3 deposition, proteinuria, and glomerular macrophage infiltrates. None of the compounds caused DNA autoantibody production or glomerulonephritis in MRL wild-type mice. The role of CpG-DNA to trigger lupus nephritis in MRLlpr/lpr mice was found to relate to its potent immunostimulatory effects at multiple levels: B cell IL12p40 production, B cell proliferation, double-stranded DNA autoantibody secretion, and dendritic cell IFN-α production. The induction of lupus nephritis by CpG-DNA is motif specific and could be prevented by co-injection of inhibitory DNA. In summary, among the ligands tested, CpG-DNA triggers lupus nephritis in genetically predisposed hosts. These data support the concept that systemic lupus erythematosus is triggered by pathogens that release CG-rich DNA.
Introd

CausticSymmetry wrote:
Last, but not least, Lupus always involves adrenal problems. So while addressing that

tooyoung wrote:

CausticSymmetry wrote:
Last, but not least, Lupus always involves adrenal problems. So while addressing that

CS, what do I need to address adrenals? Things I take that I think are beneficial to the adrenals are brewers yeast, magnesium, ashwaghanda, vit c and salt. Take another loads of supps but not sure they're of any benefit to the adrenals. Planning a DMSA and humifulvate metal chelation when I've got to time to dose at nights.

Am I missing anything major?

aI used to think that I got waves of adrenal fatigue now I'm not so sure anymore, I upped my sea salt intake by a bit and those problems went away so I think perhaps that it was just low blood pressure, any comment CS?