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Published online before print September 22, 2006

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© by The Society for Leukocyte Biology
Journal of Leukocyte Biology, doi:10.1189/jlb.1005582

Received for publication October 15, 2005.
Revised June 25, 2006.
Accepted for publication July 20, 2006.

Article

Mycobacteria-primed macrophages and dendritic cells induce an up-regulation of complement C5a anaphylatoxin receptor (CD88) in CD3+ murine T cells

Mary Anne Connelly ^*, Rachel A. Moulton ^*, Amanda K. Smith ^*, Devin R. Lindsey ^*, Meenal Sinha , Rick A. Wetsel , and Chinnaswamy Jagannath ^*@

*Department of Pathology and Laboratory Medicine, University of Texas Health Sciences Center, Houston, Texas, USA; and Institute of Molecular Medicine, Houston, Texas, USA

^@ To whom correspondence should be addressed. E-mail: chinnaswamy.jagannath{at}uth.tmc.edu.

	Abstract

Complement C5a anaphylatoxin is a potent activator of macrophages, neutrophils, and dendritic cells (DC) and binds the C5a receptor (C5a-R; CD88). Although C5a is chemotactic for T cells, expression of C5a-R on murine T cells has been disputed. We report here that naïve, Con A-activated, and cytokine (IL-12, IL-18)-stimulated murine CD3+ T cells from three strains of mice [C57Bl/6, B10.nSn (C5^+/+), B10.on (C5^-/-)] lacked C5a-R, as evaluated by immunophenotyping with an anti-C5a-R mAb. Ligation of CD3 induced a modest up-regulation with 3% of CD3+ T cells expressing cell surface C5a-R. T cells primed by APC differentiate into effector T cells. Activation of mycobacteria [bacillus Calmette-Guerin (BCG)]-sensitized T cells through MHC II and TCR interactions via BCG-infected macrophages enhanced the expression of C5a-R with 14% of CD3+ T cells positive for C5a-R. Comparable expression was found in C5^+/+ as well as C5^-/- strains of mice (14% and 15%, respectively). Furthermore, anti-CD3-activated T cells were primed by BCG-infected DC, and a larger proportion of the primed T cells expressed C5a-R (30-40%). Finally, mice infected with BCG showed significant numbers of CD3+ T cells expressing C5a-R in the spleens during infection. As APC, such as macrophages and DC, can secrete C5 and cleave C5 to C5a and C5b through a peptidase, we suggest that macrophage and DC-T cell interactions can up-regulate C5a-R on T cells through MHC II-TCR and provide a C5a peptide for additional local activation of T cells via C5a-R.

Key Words: macrophages • BCG • mouse

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