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Title: Blockade of CTLA-4 (CD152) enhances the murine antibody response to pneumococcal capsular polysaccharides
Authors: Boudewijns, Michaël ×
Jeurissen, Axel
Wuyts, Margaretha
Moens, Leen
Boon, Louis
Van Neerven, Joost J
Kasran, Ahmad
Overbergh, Lutgart
Lenaerts, Caroline
Waer, Mark
Mathieu, Chantal
Ceuppens, Jan
Bossuyt, Xavier #
Issue Date: Nov-2005
Publisher: Liss
Series Title: Journal of Leukocyte Biology vol:78 issue:5 pages:1060-1069
Abstract: The capsular polysaccharides (caps-PS) of Streptococcus pneumoniae are classified as thymus-independent antigens. Nevertheless, T lymphocytes can modulate the antibody response to caps-PS. In this study, we show that anticytotoxic T lymphocyte-associated antigen 4 (CTLA-4) treatment, along with administration of caps-PS to BALB/c mice, resulted in a dose-dependent generation of a strong caps-PS-specific antibody response. Anti-CTLA-4 treatment had no effect on the immunoglobulin G (IgG) antibody production in athymic nu/nu mice. Anti-CTLA-4 treatment stimulated the IgG antibody production in severe combined immunodeficiency (SCID)/SCID mice reconstituted with CTLA-4(-/-) B lymphocytes and wild-type T lymphocytes. This excluded the possibility that anti-CTLA-4 enhanced antibody production by direct interaction with B lymphocytes. Anti-CTLA-4 treatment enhanced the antibody production in SCID/SCID mice reconstituted with B lymphocytes and CD4(+) and CD8(+) T lymphocytes but not in SCID/SCID mice reconstituted with B lymphocytes in the absence of CD4(+) and/or CD8(+) cells. Administration of anti-CTLA-4 in BALB/c mice but not in nu/nu mice resulted in a markedly increased production of interleukin (IL)-2, IL-4, and interferon-gamma. Taken together, these data strongly suggest a role of T lymphocytes and CTLA-4 in the regulation of the antibody response to caps-PS.
ISSN: 0741-5400
Publication status: published
KU Leuven publication type: IT
Appears in Collections:Laboratory of Clinical Bacteriology and Mycology
Laboratory of Clinical Immunology
Clinical and Experimental Endocrinology
Laboratory of Nephrology
Laboratory of Experimental Transplantation
Experimental Laboratory Immunology
× corresponding author
# (joint) last author

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