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*
Department of Immunology, National Children’s Medical Research Center, Tokyo, Japan;
Department of Oral and Maxillo-facial Surgery, Tokyo Medical and Dental University, Tokyo, Japan;
Division of Pathobiology,
Division of Haematology, Department of Internal Medicine, and
¶
Department of Immunology, Juntendo University School of Medicine, Tokyo, Japan
CTLA-4 (CD152) is thought to be a negative regulator of T cell
activation. Little is known about the function of CTLA-4 in Th2-type
immune responses. We have investigated the effect of initial treatment
with anti-CTLA-4 mAb on murine chronic graft-vs-host disease.
Transfer of parental BALB/c splenocytes into C57BL/6 x BALB/c
F1 mice induced serum IgE production, IL-4 expression by
donor CD4+ T cells, and host allo-Ag-specific IgG1
production at 6–9 wk after transfer. Treatment with anti-CTLA-4
mAb for the initial 2 wk significantly reduced IgE and IgG1 production
and IL-4 expression. Analysis of the splenic phenotype revealed the
enhancement of donor T cell expansion, especially within the CD8
subset, and the elimination of host cells early after anti-CTLA-4
mAb treatment. This treatment did not affect early IFN-
expression
by CD4+ and CD8+ T cells and anti-host
cytolytic activity. Thus, blockade of CTLA-4 greatly enhanced
CD8+ T cell expansion, and this may result in the
regulation of consequent Th2-mediated humoral immune responses. These
findings suggest a new approach for regulating IgE-mediated allergic
immune responses by blockade of CTLA-4 during a critical period of Ag
sensitization.
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