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The Complement System In MS Abstracts -02

  1. The Complement protein Properdin binds Apoptotic T-Cells and promotes Complement activation and Phagocytosis
    Proc Natl Acad Sci USA 2008 Jul 1;105(26):9023-9028

  2. Immunoglobulins and Complement in postmortem Multiple Sclerosis tissue
    Ann Neurol 2009 Jan;65(1):32-46


The Complement Protein Properdin Binds Apoptotic T-Cells And Promotes Complement Activation And Phagocytosis

Kemper C, Mitchell LM, Zhang L, Hourcade DE
Proc Natl Acad Sci USA 2008 Jul 1;105(26):9023-9028
Washington University School of Medicine, Division of Rheumatology, and Department of Pathology and Immunology, Department of Medicine, St. Louis, MO 63110
PMID# 18579773

Apoptotic cells must be rapidly eliminated to avoid harmful inflammatory and Autoimmune reactions. Innate Immunity is designed/poised to identify dying cells by their unique surface-associated molecular patterns.

Here we demonstrate for the first time, to our knowledge, that the human Complement protein Properdin binds to early Apoptotic T-Cells and initiates Complement activation, leading to C3b Opsonization and ingestion by Phagocytic Cells.

Properdin binding was facilitated by the GlycoSaminoGlycan chains of surface proteoglycans.

Properdin released by activated Neutrophils was particularly effective at recognition of Apoptotic T-Cells, whereas the binding activity of Properdin in the Serum appeared to be inhibited.

"Properdin tagging" of Apoptotic T-Cells also induced their uptake by Phagocytes independent of Complement activation or other Complement proteins.

Although our findings were made primarily with Apoptotic T-Cells, they suggest that Properdin could play a similar role during Apoptosis of other cell types.


Immunoglobulins And Complement In Postmortem Multiple Sclerosis Tissue

Barnett MH, Parratt JD, Cho ES, Prineas JW
Ann Neurol 2009 Jan;65(1):32-46
University of Sydney, Department of Medicine, Institute of Clinical NeuroSciences, New South Wales, Australia
PMID# 19194879

To identify evidence of a discrete, specific Immune Response in Multiple Sclerosis (MS) by analyzing the distribution of ImmunoGlobulins and Complement in tissue derived from cases of MS.

And from control inflammatory White Matter diseases known to express Viral and AutoAntigens in the Brain and Spinal Cord.

Autopsy tissue from 25 MS patients and 24 patients with Other Neurological Diseases was examined ImmunoHistoChemically for ImmunoGlobulins and activated Complement (C3d and C9neo).

In tissue remote from focal lesions in MS and Other Neurological Diseases, IgG was detected in many normal structures but not in Myelin or ramified Microglia.

Disrupted Myelin in areas of active Myelin breakdown and in Phagocytes stained positively for C3d and C9neo, and equivocally for IgG in MS and all Other Neurological Diseases examined, including Ischemic Infarcts.

Disease-specific deposits of IgG or Complement were detected in;

  1. Virus-infected cells in Progressive Multifocal Leukoencephalopathy (PML),
  2. Subacute Sclerosing Panencephalitis, and
  3. CytoMegaloVirus Encephalitis;
  4. Glial-limiting membranes in NeuroMyelitis Optica; and
  5. Senile plaques in Alzheimer's Dementia.

Specific to MS were unusual Microglial nodules containing short, linear deposits of activated Complement (C3d) on partly DeMyelinated Axons located in Normal-Appearing PeriPlaque White Matter.

IgG and Complement immunostaining of disrupted Myelin in MS lesions, frequently cited as.

An indication of pathogenic Anti-Myelin AntiBodies, is a nonspecific feature that cannot be interpreted as evidence of a distinct pathogenesis or serve to define particular variants of the disease.

The unusual Microglial nodules described in this study may constitute a specific biomarker with pathogenetic significance in MS.

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