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Depletion of Specific Cell Populations by Complement Depletion
Published on: February 5, 2010
Complement-dependent T-cell lymphopenia caused by thymocyte deletion of the membrane complement regulator Crry
Takashi Miwa1, Lin Zhou, Yuko Kimura
1Institute for Translational Medicine and Therapeutics and Department of Pharmacology, University of Pennsylvania School of Medicine, Philadelphia, PA 19104, USA.
Blood
|January 13, 2009
Summary
Complement regulator Crry is vital for mature T-cell survival in the periphery. Crry-deficient T cells are eliminated outside the thymus due to complement attack, highlighting the thymus as a complement-privileged site.
Area of Science:
- Immunology
- Complement System Biology
- T-cell Biology
Background:
- Complement lysis is a common method for purifying lymphocytes in vitro.
- Mechanisms by which lymphocytes evade complement attack in vivo remain unclear.
Purpose of the Study:
- To investigate the role of the membrane complement regulator Crry in T-cell survival in vivo.
- To determine how T cells escape complement-mediated injury in the thymus and periphery.
Main Methods:
- Conditional gene targeting of the Crry gene in murine thymocytes.
- Analysis of T-cell populations in the thymus and periphery of Crry-deficient mice.
- Assessment of complement-mediated injury and elimination mechanisms.
Main Results:
- Conditional deletion of Crry in thymocytes resulted in peripheral T-cell lymphopenia.
- Crry-deficient T cells survived in the thymus due to low intrathymic complement activity, despite hypersensitivity to complement.
- Elimination of Crry-deficient T cells in the periphery involved C3 and macrophages, but not C5.
Conclusions:
- Crry is essential for the survival of mature T cells in the peripheral circulation.
- The thymus functions as a complement-privileged site, protecting developing T cells from complement-mediated damage.
- These findings have potential implications for developing complement-based antitumor therapies.
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