Immune responses specific for exogenous antigens are initiated by professional antigen-presenting cells (APCs). Typified by the dendritic cell, APCs have several key characteristics that render them suitable for this role. First, APCs ‘survey’ their environs by engulfing particulate and fluid matter. Second, APCs traffic to T-cell-rich regions of the lymphoid tissue and display processed antigenic fragments of engulfed matter on their cell surface in conjunction with MHC class II. Finally, through binding of the MHC-class-II–antigen complex to the T-cell receptor (TCR), coupled with the additional expression of costimulatory molecules and directed secretion of regulatory cytokines, APCs activate and polarize cognate CD4+ T cells.Activated CD4+ T cells and other leukocytes are responsible for the effector phase of specific immunity. In tissues such as the skin, gastrointestinal system and lung, eosinophils are a predominant cellular feature of this response. In particular, eosinophils are thought to be key players in allergic disease and the resolution of parasitic infection, by virtue of their release of proinflammatory molecules (including cytokines) and granular proteins (such as peroxidase). However, as highlighted by a recent publication from the laboratories of Paul Foster, there is emerging evidence that eosinophils might participate also in the inductive phase of antigen-specific immunity.In their paper, J. MacKenzie et al. 1xEosinophils promote allergic disease of the lung by regulating CD4+ Th2 lymphocyte function. MacKenzie, J. et al. J. Immunol. 2001; 167: 3146–3155PubMedSee all References1 use a murine model of ovalbumin allergy in the lung to highlight the features of eosinophils that suggest they might act as APCs. In response to provocation of the airways of allergic mice with ovalbumin, eosinophils were found to accumulate in the blood and airways, take up and process ovalbumin and, subsequently, migrate through the pulmonary parenchyma to lung-associated lymph nodes. Furthermore, eosinophils purified from the pulmonary lumen of ovalbumin-challenged allergic mice expressed MHC class II and the costimulatory molecules CD80 and CD86. Under in vitro culture conditions, these eosinophils could induce the proliferation of sensitized CD4+ T cells and promote the secretion of T helper 2 (Th2) cytokines (although these were not proven to originate from the T cells themselves). Finally, the passive transfer of ovalbumin-loaded eosinophils to naive recipients was found to predispose to Th2-mediated allergic disease of the lung upon later ovalbumin challenge, suggesting that eosinophils can prime naive T cells.This publication, in conjunction with others cited therein, provides evidence of the capacity of eosinophils to act as APCs. Whether eosinophils are involved routinely in initiating new antigen-specific immunity or, merely, in amplifying existing responses remains to be determined. Interestingly, the current studies found no change in the levels of specific antibodies in response to the passive transfer of ovalbumin-loaded eosinophils and later ovalbumin challenge in naive mice, suggesting that, at least in terms of priming for antibody production, eosinophils are relatively poor APCs. However, in the context of allergy, eosinophils acting as APCs might play a crucial role in the exacerbation of existing Th2-polarized specific immunity by regulating CD4+ T-cell function within the pulmonary microenvironment.