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*
Laboratory of Organ and System Pathophysiology, Istituto Superiore di Sanità, Rome, Italy;
Institute of General Pathology, Catholic University, Rome, Italy; and
Roche Milano Ricerche, Milan, Italy
Microglia and astrocytes, two glial cell populations of the central
nervous system, present Ag and stimulate T cell proliferation, but it
is unclear whether they preferentially activate Th1 or Th2 responses.
We have investigated the efficiency of microglia and astrocytes in the
presentation of OVA peptide 323-339 or native OVA to Th1 and Th2 cell
lines from DO11.10 TCR transgenic mice. Upon stimulation with IFN-
,
microglia express MHC class II molecules, CD40, and ICAM-1 and
efficiently present OVA 323-339, leading to T cell proliferation and
production of IL-2 and IFN- by Th1 and of IL-4 by Th2 cells.
IFN--treated astrocytes, which express MHC class II and ICAM-1,
present OVA 323-339 less efficiently to Th1 cells but are as efficient
as microglia in inducing IL-4 secretion by Th2 cells. However,
astrocytes are much less potent than microglia in presenting naturally
processed OVA peptide to either T cell subset, indicating inefficient
Ag processing. The capacity of astrocytes and microglia to stimulate
Th1 and Th2 cells depends on their MHC class II expression and does not
involve ICAM-1, B7-1, or B7-2 molecules. However, CD40-CD40L
interactions contribute to Th1 activation by microglia. These data
suggest that microglia may play a role in the activation of Th1 and Th2
cells, whereas astrocytes would restimulate mainly Th2 responses in the
presence of appropriate peptides. This differential capacity of brain
APC to restimulate Th1 and Th2 responses may contribute to the
reactivation and regulation of local inflammatory processes during
infectious and autoimmune diseases.
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