ALL2, a Novel Gene, Has a Distinct Role in pH Regulation in Cryptococcus neoformans
Cryptococcus neoformans, a facultative intracellular fungal pathogen, causes life-threatening meningoencephalitis. Its capsule and ability to replicate in the acidic phagolysosome contribute to C. neoformans resilience in the host. Jain et al. previously reported that loss of allergen 1 (ALL1) results in a shorter viscous exopolysaccharide, hypervirulence, and altered iron homeostasis. This group now reports (p. 439–451) that loss of a coregulated gene, allergen 2 (ALL2), results in a less viscous exopolysaccharide, hypovirulence, and impaired intracellular pH maintenance, in contrast to the phenotypes resulting from loss of ALL1. Thus, C. neoformans, a human-pathogenic basidiomycete, may have evolved a unique set of virulence-associated genes that contribute to its resilience in the host.
Antimycobacterial Activities and Antigen-Presenting Functions of γ9δ2 T Cells
γ9δ2 T cells comprise only 3% to 5% of total human peripheral blood lymphocytes, and yet they expand to large numbers after exposure to antigen. Abate et al. (p. 580–589) describe the ability of a γ9δ2 T cell line to inhibit intracellular mycobacteria and enhance αβ T cell responses. Mycobacterium-specific γ9δ2 T cells potently inhibit intracellular mycobacteria in a pathogen-specific manner. γ9δ2 T cells also enhance the expansion and direct antimycobacterial activities of αβ T cells through CD40-CD40 ligand interactions. In contrast with previous reports, this group demonstrates that both γ9δ2 T cells and CD4+ αβ T cells provide potent immune-enhancing/antigen-presenting cell functions.
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