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Therapeutic modalities aimed at increasing phagocyte numbers, such as granulocyte transfusions, stimulating the immune response, such as administration of haematopoietic growth factors and other proinflammatory cytokines, or indirectly augmenting immune function have shown promising results in Parvulin the preclinical setting. Because of the rarity of the infections, multicentre clinical trials are needed to demonstrate the efficacy and safety of the new immunomodulating approaches. Invasive fungal infections constitute an important cause of morbidity and mortality, especially in immunocompromised patients. Although Candida spp., Aspergillus spp. and Cryptococcus neoformans are responsible for the bulk of invasive fungal infections, other less common but problematic fungal pathogens also cause significant morbidity and mortality [1]. Among the emerging pathogens with worldwide distribution that are appearing with increasing frequency are the group of non-septate Mucormycotina [2], and septate filamentous fungi (such as Fusarium spp. and Scedosporium spp.) [1]. see more These fungal pathogens mainly affect immunocompromised hosts, such as neutropenic patients with haematological malignancies, recipients of haemotopoietic stem cell transplants (HSCTs) or solid organ transplants, patients with diabetes mellitus and ketoacidosis, premature infants, and patients with iron overload [1,2]. Although conventional antifungal therapy remains the treatment of choice, it is becoming more difficult to successfully manage these emerging invasive fungal infections. Among the factors that complicate the efficacy of antifungal treatment of these pathogens are the inherent resistance of these fungi (Fusarium spp. and Scedosporium spp. are innately resistant to most available antifungal agents), the appearance of resistant fungal strains, the adverse effects associated with antifungal chemotherapy, and the failure of antifungal therapy to sterilize infected organs [3�C5]. Therefore, given the limitations of the current antifungal armamentarium, approaches that target the host through manipulations to augment the host immune response could provide a helpful supplement to conventional treatment options. In this review, we summarize the current state of knowledge about the immunotherapeutic options for mucormycosis, VE-821 ic50 scedoporiosis, and fusariosis. Mucormycosis is caused by fungi of the order Mucorales and the family Mucoraceae [6]. In the recent reclassification, all of the agents of mucormycosis have been placed under the subphylum Mucormycotina [7]. Rhizopus, Mucor and Lichtheimia (formerly Absidia) are the most common genera causing mucormysosis, accounting for 70�C80% of all cases, whereas Cunninghamella, Apophysomyces, Saksenaea, Rhizomucor, Cokeromyces, Actinomucor and Syncephalastrum are responsible for