[Pathogenesis of pneumocystis carinii pneumonia]

Pneumocystis carinii is a ubiquitous fungus and opportunistic resident of the bronchoalveolar lumen of men and a variety of other mammalian species. This microorganism replicates under immunosuppressive conditions, ultimately resulting in lethal pneumonia (PcP) if left untreated. In the past decade, considerable progress has been made concerning the understanding of the underlying pathogenic mechanisms of this infection, mostly with the help of animal models such as SCID (severe combined immunodeficiency) or gene-knock-out mice. Partially conflicting data derived from animal studies lead to the assumption that there is no single relevant model for PcP. The T cell-mediated branch of the immune system is recognised as the major component in the host's ability to resist or overcome an infection with P. carinii. Natural, nonspecific immune mechanisms involving mononuclear phagocytes and elaborating a variety of cytokines and other immunomediators play an important role in initiating the immunoresponse as well as in its effector phase, but it is the CD4+ T lymphocytes which are essential for coordinating the complete eradication of this pathogen. The biological function and immunological effects of antigens expressed on the surface of or secreted by P. carinii organisms is not yet fully known. Hopefully, characterisation of these molecules, clarification of their immunological properties and the evaluation of the interactions between humoral and cellular as well as specific and nonspecific parts of the immune system will lead to new insights into the pathogenesis of P. carinii pneumonia.