Abstract
Cryptococcosis is a systemic fungal infection caused by Cryptococcus neoformans. In immunocompetent patients, cryptococcal infection is often confined to the lungs. In immunocompromised individuals, C. neoformans may cause life-threatening illness, either from novel exposure or through reactivation of a previously acquired latent infection. For example, cryptococcal meningitis is a severe clinical disease that can manifest in people that are immunocompromised due to AIDS. The major constituents of the Cryptococcus polysaccharide capsule, glucuronoxylomannan (GXM), and galactoxylomannan (GalXM), also known as glucuronoxylomanogalactan (GXMGal), are considered the primary virulence factors of Cryptococcus. Despite the predominance of GXM in the polysaccharide capsule, GalXM has more robust immunomodulatory effects on host cellular immunity. This review summarizes current knowledge regarding host-Crytococcus neoformans interactions and the role of capsular polysaccharides in host immunomodulation. Future studies will likely facilitate a better understanding of the mechanisms involved in antigenic recognition and host immune response to C. neoformans and lead to the development of new therapeutic pathways for cryptococcal infection.
Highlights
In Cryptococcus neoformans, capsular polysaccharides are located externally to the cell wall
Biochemical studies have shown that the C. neoformans capsule primarily comprises glucuronoxylomannan (GXM), representing ∼88% of the capsule
The GalXM consists of an α-(1→6)-galactan backbone with galactomannan side chains that are further substituted with variable numbers of xylose and Immunomodulation Induced by Cryptococcus neoformans Polysaccharides glucuronic acid residues [1]
Summary
In Cryptococcus neoformans, capsular polysaccharides are located externally to the cell wall. The production of inflammatory mediators induces the death of C. neoformans potentiating the antimicrobial activity of immune cells [7,8,9,10,11,12]. Both dendritic cells and CD4+ T cells were detected in bronchoalveolar infiltrate from lungs of C. neoformans infected mice This phenomenon coincided with increased expression of IL-12 cytokines from both subunits (p40 and p35) and the presence of IFN-γ in the lung homogenate [67]. C. neoformans infection is normally controlled by cell-mediated immunity in immunocompetent patients who develop a Th1 response following the production of IL-12, TNF-α, IFN-γ, and NO [5, 10, 68,69,70]. Recent studies with the cryptococcosis murine model have demonstrated that Th1 and Th17 subtype responses are associated with disease protection and Th2 responses are deleterious for the host [77,78,79]
Sign-in/Register to view highlights & summary Sign-in/Register to access full text options 
Free) 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a call
