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Roles of PI3K isoforms in lymphocyte development and function

Reference	BBS/E/B/0000C236
Principal Investigator / Supervisor	Professor Klaus Okkenhaug
Co-Investigators / Co-Supervisors
Institution	Babraham Institute
Department	Babraham Institute Department
Funding type	Research
Value (£)	1,810,597
Status	Completed
Type	Institute Project
Start date	19/09/2008
End date	31/03/2012
Duration	43 months

Abstract

Cells of the immune system constantly monitor their local environment for evidence of infection. B and T lymphocytes (types of white blood cell) 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, multiple sclerosis, juvenile diabetes, systemic lupus erythematosus and other diseases. Phosphoinositide 3-kinases (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 p110?, 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 p110? and hence dampen harmful immune responses. More recently we have investigated how two related enzymes, p110? and p110? c,oooperate with p110? to regulate immune responses. This work has revealed a level of redundancy (thave a similar role) between p110? and p110?, whereas p110? is not redundant with p110?. Instead, recent work suggests that p110? may be redundant with p110?. Thus further work will focus on thidentifying how p110? and p110? regulate PI3K signalling downstream of tyrosine kinase linked receptors and how p110? and p110? contribute to G-protein coupled receptor signalling.

Summary

unavailable

Committee	Closed Committee - Biochemistry & Cell Biology (BCB)
Research Topics	Immunology
Research Priority	X – Research Priority information not available
Research Initiative	X - not in an Initiative
Funding Scheme	X – not Funded via a specific Funding Scheme

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