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* Institut für Medizinische Immunologie, Charité-Campus Mitte, Universitätsmedizin Berlin, Berlin, Germany;
GenPat77 Pharmacogenetics AG, Berlin, Germany;
Kekulé-Institut für Organische Chemie und Biochemie der Universität Bonn, Bonn, Germany;
Molekulare Pathologie, Heinrich-Pette-Institut, Hamburg, Germany; and
¶ Division of Gastroenterology, Brigham and Women’s Hospital, Boston, MA 02115
The membrane protein T cell immune response cDNA 7 (TIRC7) was recently identified and was shown to play an important role in T cell activation. To characterize the function of TIRC7 in more detail, we generated TIRC7-deficient mice by gene targeting. We observed disturbed T and B cell function both in vitro and in vivo in TIRC7–/– mice. Histologically, primary and secondary lymphoid organs showed a mixture of hypo-, hyper-, and dysplastic changes of multiple lymphohemopoietic compartments. T cells from TIRC7–/– mice exhibited significantly increased proliferation and expression of IL-2, IFN-
, and IL-4 in response to different stimuli. Resting T cells from TIRC7–/– mice exhibited decreased CD62L, but increased CD11a and CD44 expression, suggesting an in vivo expansion of memory/effector T cells. Remarkably, activated T cells from TIRC7–/– mice expressed lower levels of CTLA-4 in comparison with wild-type cells. B cells from TIRC7-deficient mice exhibited significantly higher in vitro proliferation following stimulation with anti-CD40 Ab or LPS plus IL-4. B cell hyperreactivity was reflected in vivo by elevated serum levels of various Ig classes and higher CD86 expression on B cells. Furthermore, TIRC7 deficiency resulted in an augmented delayed-type hypersensitivity response that was also reflected in increased mononuclear infiltration in the skin obtained from TIRC7-deficient mice food pads. In summary, the data strongly support an important role for TIRC7 in regulating both T and B cell responses.
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