I read with interest the clinical case reported by Hiroaki Satoh et al. and, as is known, chronic eosinophilic pneumonia (CEN) is a rare condition with distinctive presenting features, which are: the presence of cough, dyspnea, fever and pulmonary infiltrates with the presence of inflammatory cells, and eosinophil accumulation.1

In this case-report, it is associated with both the presence of antinuclear antibodies, such as anti-centromere antibodies, which show a clear non-specific autoimmune response, even knowing that the centromere antibodies related to certain conditions (scleroderma) have not been demonstrated to have a pathogenic role.2

As we have reported previously, it is unknown if the phenomenon of autoimmunity is involved in CEN as a part of itself or as a serological demonstration of overlap due to the nonspecific immune response of the host.3

Hypersensitivity responses include autoimmune diseases, directed toward self antigens. Not only Type I hypersensitivity, but also III and IV may be present in CEN, conditioning different signals of an inflammatory process as allergic or autoimmune phenomena.4

It has recently been described that the eosinophil can act as an antigen presenting cell. When presenting antigens, eosinophils provide costimulation signals to lymphocytes.

The surface membrane glycoprotein CD40 interacts with its ligand CD40-CD40L and in vivo studies have demonstrated activation and proliferation of eosinophils and mast cells associated with a Th2 cell response, suggesting that eosinophils can actively modulate the immune response with amplification of Th2, so perhaps this would be the link in relation to the autoimmune response associated with the role of the eosinophil.5

Meanwhile, research into this field goes on and for the time being we get to add one more case to those reported around the world, revealing that we still have a poor understanding of immunopathology in these interesting diseases.