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Modulatory effects of alveolar macrophages on CD4+ T-cell IL-5 responses correlate with IL-1β, IL-6, and IL-12 production

Authors


  • Supported by GlaxoWelcome Australia, The Alfred Hospital Foundation and the National Health and Medical Research Council of Australia.

E.H. Walters
Dept of Respiratory Medicine
Alfred Hospital Melbourne
Victoria 3181
Australia
Fax: 61 395298498

Abstract

Abstract

Increasing evidence suggests that the pattern of T-cell cytokine production can be modulated by antigen presenting cell (APC)-derived factors during the cell interactions. Recently, it has been shown that alveolar macrophages (AMs) from atopic asthmatics (AA) but not atopic nonasthmatics (AN) enhance interleukin (IL)-5 production by CD4+ T-cells.

The present study compared AM production of IL-1β, IL-6, and IL-12, as well as their associated functional capacity to influence IL-5 production by allergen-specific CD4+ T-cells in 10 AA, 10 AN, and nine nonatopic control subjects (C).

AMs from AA showed a relatively high production of IL-1β and IL-6 (p<0.05) and a relatively low secretion of IL-12 compared to C, whereas AMs from AN and C behaved similarly. This study confirmed previous findings that co-culture with AMs augments IL-5 production from allergen-stimulated CD4+ T-cells only in AA and not in nonasthmatics even if they are atopic. On the other hand, stimulation with allergen alone did not enhance IL-5 production by CD4+ T-cells in either AA nor AN. AM-induced changes in CD4+ T-cell IL-5 production upon allergen stimulation significantly correlated with their ability to produce IL-1β (r=0.59, p<0.01), IL-6 (r=0.56, p<0.01), and inversely with IL-12 (r= -64, p=0.002) in all atopic subjects, and even more closely with the ratio of IL-12/IL-1β (r= -0.75, p<0.001) and IL-12/IL-6 production (r= -0.81, p<0.001) in these subjects.

These findings suggest that the role of alveolar macrophages from atopic asthmatics in enhancing interleukin-5 production by allergen-specific CD4+ T-cells is due, at least partly, to their aberrant production of interleukin-1β, interleukin-6, and particularly of interleukin-12.

Eur Respir J 1999; 14: 106–112.

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