In:
The Journal of Immunology, The American Association of Immunologists, Vol. 190, No. 1_Supplement ( 2013-05-01), p. 197.13-197.13
Abstract:
We recently observed that Acanthamoeba castellanii (ACA), a free-living amoeba, has the potential to trigger central nervous system autoimmunity by generating cross-reactive T cells for multiple myelin antigens, namely, proteolipid protein (PLP) 139-151 and myelin basic protein (MBP) 89-101. Additionally, the homology model derived for human leukocyte antigen-DR2, complexed with MBP 85-99 and its mimicry epitope, predicts the possibility of generating cross-reactive T cells for human MBP 85-99 in Acanthamoeba-exposed individuals. These observations raise a question whether prior exposure to ACA infection can trigger multiple sclerosis (MS). To address this hypothesis, we extracted DNA from cerebrospinal fluid obtained from MS patients and individuals with other neurological disorders, and subjected them to PCR that amplified a 500 bp fragment of the small subunit 18S rDNA using ACA-specific primer set. We confirmed the identity of PCR products by sequencing. To provide additional evidence for a linkage of ACA to MS pathogenesis, we asked whether anti-human PLP antibody can detect amoebic rhodanese-related sulfurtransferase (RST), since this protein contains the mimicry epitope ACA 83-95 for PLP 139-151. Through western blotting and LC/MS analyses, we noted that PLP antibody binds RST, suggesting that anti-Acanthamoeba immune responses have the potential to target myelin antigens. Collectively, the data suggest a linkage of ACA infection to MS pathogenesis.
Type of Medium:
Online Resource
ISSN:
0022-1767
,
1550-6606
DOI:
10.4049/jimmunol.190.Supp.197.13
Language:
English
Publisher:
The American Association of Immunologists
Publication Date:
2013
detail.hit.zdb_id:
1475085-5
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