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IMMUNE RESPONSE against Candida
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Published: 8 years ago

IMMUNE RESPONSE against Candida

IMMUNE RESPONSE — Cell wall constituents in Candida species can evoke both humoral and cellular host immune responses during the course of infection. In addition, extracellular proteinases of C. albicans trigger immune responses locally and systemically [1]. The cell-mediated immune response is clearly important in the host defense against Candida, as reflected by the higher prevalence of infections among individuals whose cellular immune systems are impaired, although the exact mechanisms of induction of this response have not been elucidated. Interleukin (IL)-12 appears to play an important role in the development of a Th1 response to C. albicans in the mouse; IL-12 deficient mice had increased susceptibility to infection introduced via the gastrointestinal tract and also to reinfection [81]. The role of interferon (IFN)-gamma seems to be more complex [82]:

IFN-gamma knock-out mice were more susceptible to Candida infection.


Experimental infection or IL-12 administration induced a Th1 response in mice associated with IFN-gamma production.


IL-12 administration to systemically infected mice resulted in uniformly lethal disease, whereas co-administration of IFN-gamma was protective in 70 percent of animals.


In contrast, IL-10 knock-out mice displayed resistance to systemic but not gastrointestinal Candida infection [83].

Neutrophils may also contribute to host defense against Candida infection. Several studies have shown that granulocyte colony-stimulating factor (G-CSF) increased neutrophil-mediated damage to pseudohyphae of C. albicans, perhaps in association with IFN-gamma [84,85]. One study found decreased salivary flow, diminished levels of secretory IgA, and reduced activity of salivary polymorphonuclear leukocytes in the patients with oral candidiasis compared to healthy controls [86].

The role of the humoral response in preventing disease progression during Candida infection has been unclear and controversial !!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!! [87,88]. However, recently developed polyclonal and monoclonal antibodies have shown a protective effect in a mouse model of candidiasis [89,90]. Mannan-specific IgG antibodies have been shown to trigger both the classical and alternative complement pathways [91]. These findings suggest that development of a vaccine or short-term protective antibodies may be feasible. In both immunocompetent and immunocompromised mice, a vaccine against C. albicans conferred reduced fungal burden and improved survival [92]. Toll-like receptors, mainly TLR2 and TLR4, play a key role in recognition of C. albicans and the activation of the host immune response [93]. In addition, the non-toll-like receptor, Dectin-1, has been shown to induce host cellular responses following recognition of beta-glucan of the fungal cell wall [94].


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