scholarly journals Analysis of Antibody Response to the Outer Surface Protein Family in Lyme Borreliosis Patients

1998 ◽  
Vol 178 (6) ◽  
pp. 1676-1683 ◽  
Author(s):  
Stephen Batsford ◽  
Christian Rust ◽  
Uwe Neubert
Keyword(s):  
Antibody Response ◽  
Lyme Borreliosis ◽  
Outer Surface ◽  
Surface Protein ◽  
Protein Family ◽  
Outer Surface Protein

Outer surface protein E antibody response and its effect on complement factor H binding to OspE in Lyme borreliosis

2008 ◽  
Vol 10 (2) ◽  
pp. 135-142 ◽  
Author(s):  
Jaana Panelius ◽  
Taru Meri ◽  
Ilkka Seppälä ◽  
Miia Eholuoto ◽  
Antti Alitalo ◽  
...  
Keyword(s):  
Antibody Response ◽  
Lyme Borreliosis ◽  
Outer Surface ◽  
Surface Protein ◽  
Factor H ◽  
Complement Factor H ◽  
Complement Factor ◽  
Outer Surface Protein

scholarly journals The Dominant Epitope of Borrelia garinii Outer Surface Protein C Recognized by Sera from Patients with Neuroborreliosis Has a Surface-Exposed Conserved Structural Motif

1998 ◽  
Vol 66 (9) ◽  
pp. 4073-4079 ◽  
Author(s):  
Marianne J. Mathiesen ◽  
Arne Holm ◽  
Michael Christiansen ◽  
Jens Blom ◽  
Klaus Hansen ◽  
...  
Keyword(s):  
B Cells ◽  
Lyme Borreliosis ◽  
Outer Surface ◽  
Protein C ◽  
Surface Protein ◽  
Terminal Region ◽  
Structural Motif ◽  
High Avidity ◽  
Binding Studies ◽  
Outer Surface Protein

ABSTRACT Epitope mapping of outer surface protein C (OspC) by using sera from patients with neuroborreliosis led to the identification of one single major immunodominant epitope within the C-terminal 10 amino acid residues. Peptide binding studies and alanine replacement scanning of the C-terminal decapeptide, PVVAESPKKP, revealed a critical role for the PKKP sequence and its terminal carboxyl group for the binding of immunoglobulin M (IgM) antibodies from patients with Lyme borreliosis. Electron microscopy of antibody-labeled spirochetes indicated that the C-terminal region is exposed on the surface of the spirochete. Based on homology to proteins of known function, this region most probably adopts a polyproline II-like helix, which is found in surface-exposed structures involved in protein-protein interactions. This structural motif is highly conserved in Borrelia species causing Lyme borreliosis and subjected to purifying selection. We suggest that the abundance of the C-terminal region of OspC on the surface of B. burgdorferi allows a multimeric high-avidity interaction between the spirochete and surface Igs on B cells. The resulting cross-linking of surface Igs on B cells may induce a T-cell-independent B-cell activation without IgM-to-IgG switching, thus explaining the lack of IgG antibodies to OspC in neuroborreliosis.

scholarly journals Production of Borreliacidal Antibody to Outer Surface Protein A In Vitro and Modulation by Interleukin-4

2000 ◽  
Vol 68 (10) ◽  
pp. 5496-5501 ◽  
Author(s):  
Erik L. Munson ◽  
Brian K. Du Chateau ◽  
Dean A. Jobe ◽  
Steven D. Lovrich ◽  
Steven M. Callister ◽  
...  
Keyword(s):  
Lymph Node ◽  
Antibody Response ◽  
Outer Surface ◽  
Protein A ◽  
Surface Protein ◽  
Interleukin 4 ◽  
Outer Surface Protein A ◽  
Outer Surface Protein ◽  
Lymph Node Cells

ABSTRACT Borreliacidal antibody production is one of several parameters for establishing the effectiveness of Borrelia burgdorferivaccines. The production of borreliacidal antibody was studied in vitro by culturing immune lymph node cells with macrophages and B. burgdorferi. We showed that borreliacidal antibody, directed primarily against outer surface protein A (OspA), was readily produced by lymph node cells obtained from C3H/HeJ mice vaccinated with formalin-inactivated B. burgdorferi in aluminum hydroxide, but not recombinant OspA. Anti-OspA borreliacidal antibody was detected in supernatants of cultures of lymph node cells obtained on day 7 after vaccination, peaked on day 17, and rapidly declined. The borreliacidal activity was attributable to immunoglobulin G1 (IgG1), IgG2a, and IgG2b antibodies. When lymph node cells were treated with interleukin-4 (IL-4), production of borreliacidal antibody was inhibited but was unaffected by treatment with anti-IL-4 antibodies. These results suggest that other cytokines, but not IL-4, are mainly responsible for production of the secondary borreliacidal antibody response.

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