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-Induced Protein-10 Production1
* Institut National de la Santé et de la Recherche Médicale Unité 416, Institut Pasteur de Lille, Lille, France;
Institut National de la Santé et de la Recherche Médicale Unité 454, Montpellier, France; and
Clinique des Maladies Respiratoires et Center Hospitalier Régional et Universitaire de Lille, Lille, France
Diesel exhausts and their associated organic compounds may be
involved in the recent increase in the prevalence of allergic
disorders, through their ability to favor a type 2 immune response.
Type 2 T cells have been shown to be preferentially recruited by the
chemokines eotaxin (CCL11), macrophage-derived chemokine (MDC, CCL22),
and thymus activation-regulated chemokine (CCL17) through their
interaction with CCR3 and CCR4, respectively, whereas type 1 T cells
are mainly recruited by IFN-
-induced protein-10 (CXCL10) through
CXCR3 binding. The aim of the study was to evaluate the effect of
diesel exposure on the expression of chemokines involved in type 1 and
2 T cell recruitment. PBMC and alveolar macrophages from house dust
mite allergic patients were incubated with combinations of diesel
extracts and Der p 1 allergen, and chemokine production was
analyzed. Diesel exposure alone decreased the constitutive IP-10
production, while it further augmented allergen-induced MDC production,
resulting in a significantly increased capacity to chemoattract human
Th2, but not Th1 clones. Inhibition experiments with anti-type 1 or
type 2 cytokine Abs as well as cytokine mRNA kinetic evaluation showed
that the chemokine variations were not dependent upon IL-4, IL-13, or
IFN- expression. In contrast, inhibition of the B7:CD28 pathway
using a CTLA-4-Ig fusion protein completely inhibited diesel-dependent
increase of allergen-induced MDC production. This inhibition was mainly
dependent upon the CD86 pathway and to a lesser extent upon the CD80
pathway. These results suggest that the exposure to diesel exhausts and
allergen may likely amplify a deleterious type 2 immune response via a
differential regulation of chemokine production through the CD28
pathway.
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