Use this URL to cite or link to this record in EThOS: http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.485808
Title: Regulation through mimicry : the milk protein butyrophilin1a1 (BTN1a1) and its influence on the immune repertoire
Author: Berer, Kerstin
ISNI:       0000 0001 3460 859X
Awarding Body: University of Aberdeen
Current Institution: University of Aberdeen
Date of Award: 2007
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Abstract:
Sensitization to the autologous milk protein butyrophilin1a1 (BTN1a1) expands a pre-existing, regulatory T cell response which cross-reacts with myelin oligodendrocyte glycoprotein (MOG), an important candidate autoantigen in multiple sclerosis (MS). This regulatory T cell population is associated with the production of high levels of IL-10 and is able to suppress proliferation of MOG-specific T cells in vitro, and to abrogate disease-severity in C57BL/6 mice with MOG-induced experimental autoimmune encephalomyelitis (EAE). These findings led us to speculate that postnatal induction of regulatory T cell responses by BTN1a1 in the mother's milk is a factor that may determine susceptibility to MOG-induced EAE in adulthood. We investigated this hypothesis using BTN1a1-deficient (BTN1a1-/-) C57BL/6 mice and wild-type (WT) littermates. Earlier onset of disease and higher disease-severity clearly indicate an increased susceptibility to MOG-induced EAE in BTN1s1 -/- mice. This was associated with higher inflammatory and demyelinating indices in BTN1a1-/- mice compared to their WT littermates. Moreover, functional analysis of MOG-specific T cells in BTN1a1-/- mice revealed a marked increase in the production of encephalitogenic cytokines (IL-17, IFN-Y and IL-6), while the synthesis of IL-10 was consistently decreased. Collectively, our data suggest that regulatory T cell responses induced by autologous BTN1a1 play an important role in determining susceptibility to MOG-induced EAE.
Supervisor: Not available Sponsor: Not available
Qualification Name: Thesis (Ph.D.) Qualification Level: Doctoral
EThOS ID: uk.bl.ethos.485808  DOI: Not available
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