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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).