[Pathogenesis, immunobiology and epidemiology of XXXX ].

@entity1 @entity404 @entity3217 @entity1327 @entity1328 @entity791
@entity1327 is taken up by the @entity1 host via the respiratory tract. The polysaccharide capsule is regarded as the pathogenetic principle inhibiting phagocytosis of the fungus by cells of the unspecific host defense. Unspecific opsonization of Cr. n. by early phase proteins causes a rapid and successful elimination in the non-compromised host. In case of non-elimination the presence of Cr. n. capsule antigen in excess results in a downregulation of antibody formation thereby inhibiting specific opsonization. Furthermore the blockade of specific T cells and cytotoxic cells by means of free antigen and/or immunocomplexes causes a downregulation of the cellular immunity: Cr. n. antigens of different character induce T suppressor cells inhibiting cellular immunity via a cascade of effector cells and soluble factors. The @entity791 @entity1 enters @entity1328 in a state comparable to a Cr. n.-infected non- @entity791 @entity1 whose cellular immunity is already downregulated by this @entity3217 itself. Both phenomena--the @entity3217 -induced downregulation of cellular immunity as well as the @entity791 -specific lack of @entity404 helper cells and its consequences--act, therefore, synergistically in the same pathogenetic direction. This explains the fulminant development and sequel of @entity1328 typical with @entity791 @entity1 . Most probably each exposition of an @entity791 @entity1 to Cr. n. results in clinically manifest @entity1328 . The frequence of @entity1328 in @entity791 is, therefore, reflecting the general exposure of @entity1 to Cr. n. in a given region. @entity1328 in @entity791 is at least about 1000x more frequent than @entity1328 in non- @entity791 individuals.(ABSTRACT TRUNCATED AT 250 WORDS)
