Abstract
Activation of natural killer-like T (NKT) cells with the CD1d ligand alpha-galactosylceramide enhances T-dependent humoral immune responses against coadministered T-dependent Ag. At present, there is little information on the mechanisms involved other than a dependence on CD1d expression by antigen-presenting cells and/or development of the NKT subset. We therefore tested the hypothesis that direct presentation of alpha-GC by B cells was required for NKT-enhanced Ab responses against T-dependent Ag. We reconstituted B cell-deficient microMT mice with B cells from C57Bl/6 donors or CD1d(-/-) donors before immunization with NP-KLH alone or NP-KLH mixed with alpha-GC. We made the surprising observation that B-cell expression of CD1d is absolutely required for the NKT-enhanced Ab response. Our data show that the mechanism by which NKT cells enhance humoral immune responses involves interaction with CD1d-expressing B cells.
MeSH Terms
Adoptive Transfer
Animals
Antibody Formation
Antigens, CD/immunology
Antigens, CD1/genetics,immunology
Antigens, CD1d
B-Lymphocytes/immunology
Galactosylceramides/pharmacology
Humans
Killer Cells, Natural/drug effects,immunology
Lymphocyte Activation/drug effects
Mice
Mice, Knockout
Spleen/immunology
Thymus Gland/immunology
Chemicals
Antigens, CD
Antigens, CD1
Antigens, CD1d
CD1D protein, human
Galactosylceramides
alpha-galactosylceramide
Authors & Affiliations
3 authors, click to expand affiliations / ORCID
Lang Gillian A
Department of Microbiology and Immunology, University of Oklahoma Health Sciences Center, Oklahoma City, OK 73104, USA.
Devera T Scott
Lang Mark L
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