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Characterization of the B‐cell inhibitory protein factor in Ixodes ricinus tick saliva: a potential role in enhanced Borrelia burgdoferi transmission
Author(s) -
Hannier Sigrid,
Liversidge Janet,
Sternberg Jeremy M.,
Bowman Alan S.
Publication year - 2004
Publication title -
immunology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.297
H-Index - 133
eISSN - 1365-2567
pISSN - 0019-2805
DOI - 10.1111/j.1365-2567.2004.01975.x
Subject(s) - saliva , borrelia burgdorferi , biology , ricinus , borrelia , microbiology and biotechnology , lipopolysaccharide , tick , antibody , biochemistry , virology , immunology
Summary We recently described the inhibition of host B lymphocytes by Ixodes ricinus tick saliva. In this study, we characterized the factor responsible for this activity and examined the modulation of lipopolysaccharide (LPS)‐ and Borrelia burgdorferi outer surface protein (Osp)‐induced proliferation of naive murine B lymphocytes by an enriched fraction of this factor. The B‐lymphocyte inhibitory activity was destroyed by trypsin treatment, indicating that a proteinaceous factor was responsible for this activity. The removal of glutathione‐S‐transferase (GST) from tick salivary glands extracts (SGE) showed that this B‐cell inhibitory protein (BIP) was not a GST. Gel filtration liquid chromatography indicated that BIP has a native molecular weight of ≈ 18 000. An enrichment protocol, using a combination of anion‐exchange and reverse‐phase liquid chromatography, was established. BIP‐enriched fractions did not suppress T‐cell proliferation. Delayed addition of BIP‐enriched fractions, up to 7 hr after LPS addition, inhibited the proliferation of isolated B cells. BIP‐enriched fractions dramatically inhibited both OspA‐ and OspC‐induced proliferation of isolated B cells. These results strongly suggest that BIP may facilitate B. burgdorferi transmission by preventing B‐cell activation, and also highlights the potential of BIP as a therapeutic agent in B‐cell maladies.