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Expression of Signaling Lymphocytic Activation Molecule- Associated Protein Interrupts IFN- Production in Human Tuberculosis ¹

Virginia Pasquinelli^*,, María F. Quiroga^*,, Gustavo J. Martínez^*,, Liliana Castro Zorrilla, Rosa M. Musella, María M. Bracco^¶, Liliana Belmonte^¶, Alejandro Malbrán^||, Leonardo Fainboim^*,, Peter A. Sieling^# and Verónica E. García^2,*,

^* Department of Microbiology, Parasitology and Immunology, University of Buenos Aires School of Medicine, Laboratorio de Inmunogenética, Hospital de Clínicas José de San Martín, University of Buenos Aires, Department of Immunology, "Instituto de Tisioneumonología Prof. Dr. Raúl Vaccarezza," University of Buenos Aires, School of Medicine, División Tisioneumonología, Hospital FJ Muñiz, ^¶ Instituto de Investigaciones Hematológicas, Academia Nacional de Medicina, ^|| Departamento de Alergia e Inmunología, Hospital Británico, Buenos Aires, Argentina; and ^# Division of Dermatology, Department of Medicine, David Geffen School of Medicine, University of California, Los Angeles, CA 90095

Production of the Th1 cytokine IFN- by T cells is considered crucial for immunity against Mycobacterium tuberculosis infection. We evaluated IFN- production in tuberculosis in the context of signaling molecules known to regulate Th1 cytokines. Two populations of patients who have active tuberculosis were identified, based on their T cell responses to the bacterium. High responder tuberculosis patients displayed significant M. tuberculosis-dependent T cell proliferation and IFN- production, whereas low responder tuberculosis patients displayed weak or no T cell responses to M. tuberculosis. The expression of the signaling lymphocytic activation molecule (SLAM)-associated protein (SAP) on cells from tuberculosis patients was inversely correlated with IFN- production in those individuals. Moreover, patients with a nonfunctional SAP gene displayed immune responses to M. tuberculosis similar to those of high responder tuberculosis patients. In contrast to SAP, T cell expression of SLAM was directly correlated with responsiveness to M. tuberculosis Ag. Our data suggest that expression of SAP interferes with Th1 responses whereas SLAM expression contributes to Th1 cytokine responses in tuberculosis. The study further suggests that SAP and SLAM might be focal points for therapeutic modulation of T cell cytokine responses in tuberculosis.

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