Journal article
Self-Recognition of Cd1 by γ/δ T Cells: Implications for Innate Immunity
The Journal of experimental medicine, Vol.191(6), pp.937-948
03/20/2000
DOI: 10.1084/jem.191.6.937
PMID: 10727456
Abstract
The specificity of immunoglobulins and α/β T cell receptors (TCRs) provides a framework for the molecular basis of antigen recognition. Yet, evolution has preserved a separate lineage of γ/δ antigen receptors that share characteristics of both immunoglobulins and α/β TCRs but whose antigens remain poorly understood. We now show that T cells of the major tissue γ/δ T cell subset recognize nonpolymorphic CD1c molecules. These T cells proliferated in response to CD1
+
presenter cells, lysed CD1c
+
targets, and released T helper type 1 (Th1) cytokines. The CD1c-reactive γ/δ T cells were cytotoxic and used both perforin- and Fas-mediated cytotoxicity. Moreover, they produced granulysin, an important antimicrobial protein. Recognition of CD1c was TCR mediated, as recognition was transferred by transfection of the γ/δ TCR. Importantly, all CD1c-reactive γ/δ T cells express Vδ1 TCRs, the TCR expressed by most tissue γ/δ T cells. Recognition by this tissue pool of γ/δ T cells provides the human immune system with the capacity to respond rapidly to nonpolymorphic molecules on professional antigen presenting cells (APCs) in the absence of foreign antigens that may activate or eliminate the APCs. The presence of bactericidal granulysin suggests these cells may directly mediate host defense even before foreign antigen-specific T cells have differentiated.
Details
- Title: Subtitle
- Self-Recognition of Cd1 by γ/δ T Cells: Implications for Innate Immunity
- Creators
- Franca M SpadaEthan P GrantPeter J PetersMasahiko SugitaAugustín MeliánDavid S LeslieHoi K LeeElly van DonselaarDennis A HansonAlan M KrenskyOtto MajdicSteven A PorcelliCraig T MoritaMichael B Brenner
- Resource Type
- Journal article
- Publication Details
- The Journal of experimental medicine, Vol.191(6), pp.937-948
- DOI
- 10.1084/jem.191.6.937
- PMID
- 10727456
- NLM abbreviation
- J Exp Med
- ISSN
- 0022-1007
- eISSN
- 1540-9538
- Publisher
- The Rockefeller University Press
- Language
- English
- Date published
- 03/20/2000
- Academic Unit
- Immunology; Internal Medicine
- Record Identifier
- 9984094613802771
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