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B7 costimulatory ligand regulates development of the T‐cell response to Cryptococcus neoformans
Author(s) -
Claudia Monari,
Kozel Tr,
Arturo Casadevall,
Donatella Pietrella,
Barbara Palazzetti,
Anna Vecchiarelli
Publication year - 1999
Publication title -
immunology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.297
H-Index - 133
eISSN - 1365-2567
pISSN - 0019-2805
DOI - 10.1046/j.1365-2567.1999.00853.x
Subject(s) - cryptococcus neoformans , t cell , cd28 , biology , microbiology and biotechnology , secretion , monoclonal antibody , population , interleukin 2 , interleukin 4 , cell , antibody , cytokine , immunology , immune system , biochemistry , medicine , environmental health
The contribution of B7 molecules to the induction and maintenance of the T‐cell response to the human pathogenic fungus Cryptococcus neoformans was investigated. T‐cell activation by C. neoformans was regulated by B7 molecules. This costimulatory signal was necessary for initiation and maintenance of the T‐cell response, through early and late requirements for B7–CD28 interaction. Blocking B7‐2 inhibited the normal T‐cell proliferative response. This inhibition was due, in part, to a reduced capability of T cells to produce interleukin‐2 (IL‐2). In contrast, the same T‐cell population produced more interferon‐γ. Suppression of the normal lymphoproliferation and IL‐2 secretion responses to encapsulated C. neoformans by antibodies to B7 was largely reversed by addition of the monoclonal antibody 2H1, that is reactive with the major capsular polysaccharide, glucuronoxylomannan. Overall, our data indicate that B7 molecules play a critical role in T‐cell activation by C. neoformans and suggest that appropriate manipulation could drive T helper type 1 cell development.