Pulmonary Vβ4+ T Cells from Histoplasma capsulatum–Infected Mice Respond to a Homologue of Sec31 That Confers a Protective Response

• Published in: The Journal of infectious diseases Vol. 193; no. 6; pp. 888 - 897
• Main Authors: Scheckelhoff, Mark R., Deepe, George S.
• Format: Journal Article
• Language: English
• Published: Chicago, IL The University of Chicago Press 15.03.2006; University of Chicago Press
• Subjects: Biological and medical sciences; Fundamental and applied biological sciences. Psychology; Infectious diseases; Medical sciences; Microbiology; Miscellaneous; Mycology; Fungi; Infection; Vertebrata; Mammalia; Microbiology; Mouse; Rodentia; T-Lymphocyte; Histoplasma capsulatum; Fungi Imperfecti; Infected cell; Thallophyta
• ISSN: 0022-1899; 1537-6613
• DOI: 10.1086/500244

The population of Vβ4+ T cells expands in the lungs of C57BL/6 mice infected with Histoplasma capsulatum and the elimination of these cells impairs protective immunity. To determine the antigen or antigens that trigger their proliferation, Vβ4+ T cell hybridomas were generated from the lungs and spleens of infected mice. We mapped the antigenic determinants by T cell Western blot. Pulmonary and splenic T cells recognized 3 regions comprising <25, 55–70, and 125–140 kDa. The majority of hybridomas from lungs, but not from spleens, responded to the high molecular mass region. A protein from that area was identified, by amino acid sequencing, as a homologue of Sec31 from Saccharomyces cerevisiae Vaccination with recombinant Sec31 reduced fungal burden and improved survival in mice, and its efficacy was critically dependent on the presence of Vβ4+ T cells. Thus, a homologue of Sec31 is a trigger of the expansion of the Vβ4+ T cell population and is important to the generation of protective immunity