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Title: Immunological properties of microglia
Author: Hall, G. L.
Awarding Body: University of Cambridge
Current Institution: University of Cambridge
Date of Award: 1998
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This thesis examines the immunological accessory functions of neonatal rodent microglia and in particular, their response to β-IFN. β-IFN is shown to inhibit gamma-interferon (γ-IFN)-mediated induction of surface MHC class II expression on the microglia. Although the exact mechanism by which β-IFN blocks class II expression is not resolved, β-IFN- mediated inhibition of antigen presentation by γ-IFN stimulated microglia to primed T cells demonstrates the functional relevance of the effect. The ability of microglia to interact with T cells and function as antigen presenting cells is examined further. Neonatal rat microglia are shown not to be fully 'professional', that is, not able to act as stimulator cells in a mixed lymphocyte reaction but they can activate primed T cells in an antigen recall assay in such a way to propagate an immune response; microglia provide sufficient costimulation to induce primed T cells to produce cytokines and resting microglia are shown to be able to respond to these signals by activating interferon-induced transcription factors. γ-IFN is identified as the active factor within the supernatant. In addition to studying microglial-T cell interactions, the effects of β-IFN on a comprehensive range of immunological accessory and cytotoxic effector functions of the rodent microglia have been studied and the interaction of β-IFN with γ-IFN considered. Microglial proliferation, FcR expression, ability to mount a respiratory burst and to secrete TNFα and nitric oxide have been examined. Both antagonistic and synergistic effects of these cytokines are described, which in addition to the effects on class II expression described, re-emphasises the complexity of immune interactions between immunocompetent cells, cytokines and potentially beneficial immunotherapeutic agents. In the light of these findings, a possible model of action for β-IFN in MS patients is discussed.
Supervisor: Not available Sponsor: Not available
Qualification Name: Thesis (Ph.D.) Qualification Level: Doctoral
EThOS ID:  DOI: Not available