ABSTRACT
Many groups of immunosuppressed individuals are susceptible to the opportunistic pathogen Pneumocystis jiroveci. In most but not all of these hosts, the primary immune derangement is a deficiency in the number or function of T cells [1]. While there are clearly humoral immune deficiencies that predispose hosts to P. jiroveci pneumonia, such as severe combined immunodeficiency, the majority of patients diagnosed with this infection are infected with HIV or are iatrogenically immunosuppressed [2]. Despite the clinical importance of P. jiroveci pneumonia, however, major gaps persist in understanding the host immunity to this organism. A recent National Institutes of Health (NIH) consensus conference identified several such unresolved issues concerning the host immune response to P. jiroveci. One of these issues concerned identification of the essential mechanisms of immune response to P. jiroveci in HIV-infected hosts and determination of whether responses remain localized or occur systemically [2]. This uncertainty extends to understanding the roles of T cells in defense against Pneumocystis. Among extracellular organisms, study of Pneumocystis demonstrates that T cells perform unique roles in control of host defense and pulmonary inflammation. Once impairments in pulmonary host defenses are understood, novel strategies
to correct these defects may be developed for treatment and prophylaxis of Pneumocystis pneumonia [2,3].
