Award details

MRC Capacity Building Studentship: Phosphoinositide 3-kinase isoforms in immunity

ReferenceBBS/E/B/0000M979
Principal Investigator / Supervisor Professor Klaus Okkenhaug
Co-Investigators /
Co-Supervisors
Institution Babraham Institute
DepartmentBabraham Institute Department
Funding typeResearch
Value (£) 44,592
StatusCompleted
TypeInstitute Project
Start date 01/10/2004
End date 30/09/2007
Duration36 months

Abstract

Cells of the immune system constantly monitor their local environment for evidence of infection. B and T lymphocytes have evolved to distinguish self (any tissue in the organism) from non-self (infectious agents). Foreign substances, which include the chemical make-up of bacteria and viruses, stimulate B and T lymphocytes to divide rapidly and produce antibodies and other substances that help rid the body of the infectious agent. B and T cells can recall a previous encounter with a particular organism and mount a faster and more vigorous response to subsequent encounters. However, in some cases, B and T lymphocytes mistakenly recognise components of different organs as infectious agents. This mistake can lead to autoimmune diseases such as rheumatoid arthritis, muscular sclerosis, juvenile diabetes, systemic lupus erythematosus and other devastating illnesses. Much scientific research effort is therefore directed towards the goal of developing drugs that can suppress the immune system under circumstances where it is too active or where it turns against self rather than infectious agents. One approach is to interfere with the signals that are generated inside the B or T cells upon recognition of foreign substances (or self, as the case may be). Phosphoinositide 3-kinases (also known as PI3Ks) are a family of enzymes used by the cell to transmit signals from receptors on the outside of the cell to the machinery inside the cell that dictates how a cell behaves. We have previously identified one member of this family, called p110delta, which plays an important role in transmitting the signals generated when a B or T cell recognises foreign antigens. As a consequence of this discovery, pharmaceutical companies are developing drugs that can interfere with p110delta and hence dampen harmful immune responses. In this grant, we wish to investigate how two related enzymes, p110alpha and p110beta, might regulate B and T cell responses on their own, and how they might co-operate with p110delta. This work will help to provide the rationale for the development of more effective drugs against autoimmune disorders.

Summary

unavailable
Committee Closed Committee - Biochemistry & Cell Biology (BCB)
Research TopicsX – not assigned to a current Research Topic
Research PriorityX – Research Priority information not available
Research Initiative X - not in an Initiative
Funding SchemeX – not Funded via a specific Funding Scheme
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