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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


  • 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
Fax: 61 395298498



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.