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Is CD248 involved in the resolution of inflammation during development of lung sarcoidosis? and the role of adipose tissue-derived stromal cells in the survival of lymphocytes

Apta, Bonita Harriet Radha (2013)
M.Res. thesis, University of Birmingham.

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Recent findings suggest CD248 involvement in inflammation and tissue remodeling/repair. These processes occur during inflammation and fibrogenesis. Therefore we explored the role of CD248 in a mouse model of sarcoidosis. Apolipoprotein-E (ApoE) knock-out, CD248 knock-out, and double knock-out mice were fed a high-fat diet (HFD). Histological analysis was followed with immunofluorescent CD248 staining. ApoE deficiency combined with HFD induced sarcoid-like granulomas. Our results suggest CD248 involvement in the resolution of inflammation. CD248 deficiency influenced disease severity and expression increased in the sarcoid lung. CD248’s influence on resolution is a promising finding. Investigation in other models of inflammation could uncover its immunological role and therapeutic potential.

Stromal cells regulate lymphocyte homeostasis in the lymph node and are derived from adipocyte precursors in surrounding fat. Factors regulating lymphocytes in adipose tissue are unknown. We assessed the role of adipose tissue-derived stromal cells in lymphocyte survival. Lymphocyte survival in co-culture with stromal cells was examined using flow cytometry, and expression of key lymphotrophic factors was investigated with real-time PCR. Our findings suggest that pre-adipocytes in the adipose tissue stromal vascular fraction produce IL-7 and CCL19, supporting T lymphocyte survival. Comprehensive understanding of pre-adipocyte modulation of T cells, and how adipose tissue influences immune responses may facilitate development of novel therapies.

Type of Work:M.Res. thesis.
Supervisor(s):Rainger, Ed
School/Faculty:Colleges (2008 onwards) > College of Medical & Dental Sciences
Department:School of Clinical and Experimental Medicine
Subjects:RA0421 Public health. Hygiene. Preventive Medicine
RC Internal medicine
Institution:University of Birmingham
ID Code:3721
This unpublished thesis/dissertation is copyright of the author and/or third parties. The intellectual property rights of the author or third parties in respect of this work are as defined by The Copyright Designs and Patents Act 1988 or as modified by any successor legislation. Any use made of information contained in this thesis/dissertation must be in accordance with that legislation and must be properly acknowledged. Further distribution or reproduction in any format is prohibited without the permission of the copyright holder.
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