[Resistance to intestinal opportunistic infections using Cryptosporidium sp. as an example]

Cryptosporidium sp. has emerged as an important cause of intestinal opportunistic infections in immunocompromised humans, especially in HIV positive patients. The host immune responses to these infections both in humans and in animals are still poorly understood. However, experimental and clinical studies show that both humoral and cellular immune responses are essential to control the duration and severity of Cryptosporidium sp. infection. The role of specific IgM, IgG, IgA and secretory IgA remains unclear. Nevertheless, high level of IgG and IgM responses was found in ADIS patients with chronic infection. Hyperimmune bovine colostrum decreases parasite burden and severe diarrhea. Severe chronic infections have been found in hosts with selective T-cell deficiency, especially AIDS patients with low CD4+ T-cell counts (<50 cells/mm3). Moreover, it is also generally agreed that T lymphocytes are required for the resolution of both acute and chronic cryptosporidisis. Several studies suggest that IFN-gamma is very important in the control of Cryptosporidium infection; especially intestinal intraepithelial CD4+ T-cells (IEL) that produce IFN-gamma are potentially crucial mediators of host immunity to Cryptosporidium. Recent experimental studies also indicate that mice deficient in either alphabeta or gammasigma T cells are more susceptible to infection than control mice, however gammasigma T-cells have a less critical role than alphabeta T-cells. Less extensive studies investigating the role of other cells and cytokines both in the innate and cell-mediated immune responses to Cryptosporidium sp. are also discussed.