       Document 0449
 DOCN  M9610449
 TI    Biology of human TH1 and TH2 cells.
 DT    9601
 AU    Romagnani S; Division of Clinical Immunology and Allergy, University of;
       Florence, Italy.
 SO    J Clin Immunol. 1995 May;15(3):121-9. Unique Identifier : AIDSLINE
       MED/96053529
 AB    Evidence is accumulating to suggest the existence of polarized human
       T-cell responses, reminiscent of TH1 and TH2 subsets described for mouse
       T cells. Human TH1 cells preferentially develop during infections by
       intracellular bacteria and trigger phagocyte-mediated host defense,
       whereas TH2 cells, which predominate during helminthic infestations and
       in response to common environmental allergens, are responsible for
       phagocyte-independent host response. Human TH1 and TH2 cells exhibit not
       only different functional properties but probably also distinct surface
       markers; TH2, but not TH1, clones express membrane CD30 and release the
       soluble form of CD30, a member of the TNF receptor superfamily. The
       cytokine profile of natural immunity evoked by different offending
       agents in the context of different host genetic backgrounds appears to
       be the most critical factor in determining the phenotype of the
       subsequent specific response. IL-12 and IFN-alpha and gamma produced by
       macrophages and NK cells favor the development of TH1 cells, whereas the
       early production of IL-4 by a still-unidentified cell type favors the
       development of TH2 cells. Clearly, polarized human TH1 and TH2 responses
       not only play different roles in protection, they can also promote
       different immunopathological reactions. Strong and persistent TH1
       responses seen to be involved in organ-specific autoimmunity, contact
       dermatitis, and some chronic inflammatory disorders of unknown etiology.
       In contrast, polarized TH2 responses favor a reduced protection against
       the majority of infectious agents (including HIV) and, in genetically
       predisposed hosts, are responsible for triggering of allergic atopic
       disorders.
 DE    Human  Support, Non-U.S. Gov't  Th1 Cells/*IMMUNOLOGY  Th2
       Cells/*IMMUNOLOGY  JOURNAL ARTICLE  REVIEW  REVIEW, TUTORIAL

       SOURCE: National Library of Medicine.  NOTICE: This material may be
       protected by Copyright Law (Title 17, U.S.Code).

