University of BristolAutoimmune Inflammation Research

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Investigators and Projects

Lindsay Nicholson

Andrew Dick

Overview of research

T cell macrophage interactions

Properties of eye autoantigens

Inflammation and angiogenesis

Leucocyte populations in EAU

Steroid resistance

CD200 in EAU

Complement and ocular disease

Modelling Immune responses in silico

Selected References

Vision Research 2007

Vision Research 2008

Vision Research 2009

Recent Advances

Our Research

Overview of Research

This figure summarises the autoimmune process. The table shows where specific projects fit in this scheme. This figure summarises the autoimmune process. The table lists these processes and describes where specific projects fit in this scheme. The headings for the table are A:Initiation or reactivation, B: Expansion and trafficking, C: Target organ localisation, activation and damage, D: Amplification, regulation and memory generation, E: Remission and F: The whole process together





Processing of autoantigens
Recognition of autoantigens
Cross-reactive activation (molecular mimicry)
Balance of activating and inactivating signalling
Bystander activation
Analysis of T cell responses to retinal autoantigens
Role of macrophages as antigen presenting cells in the ocular environment


Regulation of cell division
Differentiation to effector phenotypes
Chemotaxis and chemokinesis
Endothelial/lymphocyte interactions
Steroid control of lymphocyte responses
Genesis and role of IL-17 specific T cells in EAU


Extra-cellular matrix/cellular interactions
Local antigen processing and presentation
Actions of soluble mediators of inflammation
Action of soluble mediators on lymphocytes and local tissue
Repair of target organ damage
Innate immune activation of macrophages
Role of TNFR1, TLR-4 and TSP-1 in the regulation of ocular inflammation
Role of complement in amplifying inflammatory responses
Effects of inflammation on retinal repair


Expansion and contraction of lymphocyte populations
Generation of autoimmune specific regulatory cells
Generation of autoantigen specific memory cells
Epigenetic control of gene expression
Lymphocyte population studies in EAU
Epigenetic control of T cell activation status


Loss of autoantigen specific lymphocytes
Local down-regulation of inflammation
Dominance of regulatory cells
Effects of immune privilege
Initiation of relapse
Role of CD200/CD200R in the downregulation of inflammation


Emergent properties that can arise in the context of the whole system Computer simulations of simplified models of immune responses

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