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Ectopically expressed PIR-B on T cells constitutively binds to MHC class I and attenuates T helper type 1 responses.
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- Additional Information
- Source:
Publisher: [Oxford University Press Country of Publication: England NLM ID: 8916182 Publication Model: Print-Electronic Cited Medium: Internet ISSN: 1460-2377 (Electronic) Linking ISSN: 09538178 NLM ISO Abbreviation: Int Immunol Subsets: MEDLINE
- Publication Information:
Original Publication: Oxford : [Oxford University Press, 1989-
- Subject Terms:
- Abstract:
Activated mature T cells induce various inhibitory receptors implicated in maintaining peripheral tolerance in response to the trans-acting ligands. Interestingly, paired Ig-like receptor (PIR)-B, an inhibitory MHC class I receptor on B cells and myeloid cells, could be involved in regulating early T cell development because epitope for PIR is detected on pre-thymic T/NK progenitors but not on thymocytes or mature T cells. We hypothesized that PIR-B is not only a regulator for T cell development but is also detrimental if expressed on mature T cells. Here we demonstrated, using PIR-B-deficient fetuses, that PIR-B is indeed expressed on the T cell progenitors but failed to identify its distinctive roles in the development. Forced expression of PIR-B in thymocytes and mature T cells also resulted in no abnormalities in development. However, upon antigenic or allogeneic stimulation, peripheral T cells with the ectopic PIR-B showed reduced T(h) type 1 responses due to the suppression of proximal TCR signaling by constitutive binding of PIR-B to MHC class I on the same cell surface. Our findings suggest that T cell expression of PIR-B with the cis-interacting MHC class I is strictly prohibited in periphery so as to secure prompt immune responses.
- Accession Number:
0 (Histocompatibility Antigens Class I)
0 (Pirb protein, mouse)
0 (Receptors, Immunologic)
82115-62-6 (Interferon-gamma)
9006-59-1 (Ovalbumin)
- Publication Date:
Date Created: 20090818 Date Completed: 20091209 Latest Revision: 20090925
- Publication Date:
20221213
- Accession Number:
10.1093/intimm/dxp081
- Accession Number:
19684158
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