The fungal genus Cryptococcus comprises a group of pathogens with considerable phenotypic and genotypic diversity that can lead to cryptococcosis in both healthy and immunocompromised individuals. With the emergence of the HIV pandemic, cryptococcosis, mainly meningoencephalitis, afflicts HIV-infected patients with severe dysfunction of T cells. It has also been reported in recipients of solid organ transplantation and in patients with autoimmune diseases who take immunosuppressive agents long-term, as well as in those with unidentified immunodeficiency. The clinical outcome of the disease is primarily determined by the immune response resulting from the interplay between the host immune system and the pathogen. Most human infections are caused by Cryptococcus neoformans, and nearly all immunological studies have focused on C. neoformans. This review provides an updated understanding of the role of adaptive immunity during infection with C. neoformans in human and animal models over the past half-decade.

Cryptococcal meningitis (CM) is a common fungal infectious disease of the central nervous system (CNS) caused by Cryptococcus neoformans and is a severe fungal disease that endangers human health. It is responsible for approximately 200,000 global deaths annually (1). C. neoformans, also known as Torula histolytica, is an encapsulated yeast that can survive in soil, pigeons, milk, and fruits. It can infect humans and animals and typically manifests as an exogenous infection; however, it may also be endogenous and opportunistic.

Cryptococcal disease, or cryptococcosis, is caused by the Cryptococcus species complex and can occur in both immunocompromised patients and healthy individuals. The Cryptococcus complex comprises seven species (2). C. neoformans and Cryptococcus deneoformans primarily cause infections in severely immunocompromised individuals, including patients with HIV/AIDS, especially those with CD4+ T-cell counts of