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J Biol Chem, Vol. 273, Issue 46, 30680-30687, November 13, 1998
From the Glycobiology Program, La Jolla Cancer Research Center, The
Burnham Institute, La Jolla, California 92037
The aberrant expression of core 2 O-glycans on T cell surface glycoproteins has been
associated with various immunodeficient syndromes such as
Wiskott-Aldrich syndrome and AIDS. To determine the effect of this
aberrant expression of core 2 O-glycans on immune
responses, we previously generated transgenic mice overexpressing core
2 
-1,6-N-acetylglucosaminyltransferase (C2GnT) in T
cells, and demonstrated that T cell primary immune responses mediated through interaction between T cells and antigen-presenting cells are
impaired in the transgenic mice (Tsuboi, S., and Fukuda, M. (1997)
EMBO J. 16, 6364-6373). In this study, we determined
whether overexpression of core 2 oligosaccharides on T cells leads to impaired humoral immune responses by B cells using the same transgenic mice. When T cells were activated, both T and B cells from the transgenic and control mice expressed an equivalent amount of CD40L and
CD40, which are, respectively, the receptor and counter-receptor for
the interaction between T and B cells. However, activated T cells from
the transgenic mice induced B cell proliferation less efficiently than
those from control mice, regardless of whether B cells were isolated
from control or the transgenic mice. This suggests that overexpression
of core 2 O-glycans on T cell surface glycoproteins renders
T cell-B cell interaction inefficient. Moreover, in the transgenic mice
both immunoglobulin isotype switching and germinal center formation
were also impaired. Taken together, these results indicate that
aberrant expression of core 2 O-glycans on T cell surface
glycoproteins results in impaired humoral immune responses due to an
impaired interaction between T and B cells.
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