Abstract

Human T helper 1 (Th1) cells develop preferentially during infections by intracellular parasites and trigger phagocyte-mediated host defence. In contrast, human Th2 cells are responsible for phagocyte-independent host response, and they predominate during helminthic infestations and in atopic humans in response to common environmental antigens. Polarized human Th1 and Th2 cell responses play different roles in protection, and they can promote different immunopathological reactions. Strong and persistent Th1 responses seem to be involved in organ-specific autoimmunity, contact dermatitis and some chronic non-allergic inflammatory disorders. Polarized Th2 responses favour reduced protection against the majority of infections, including HIV, and they are responsible for triggering allergic disorders in genetically predisposed hosts. Th1 and Th2 cells probably exhibit distinct surface markers; for example, Th2 cells express preferentially membrane CD30 and release the soluble form of CD30, which is a member of the tumour necrosis factor receptor superfamily. CD30-mediated signalling promotes the in vitro development of Th2-like cells. The expression of CD30 in HIV-infected T cells results in enhanced HIV replication, suggesting the existence of complex links among CD30 expression, production of Th2-type cytokines and immunopathogenesis of HIV infection.

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