|
|||||||||
|
|
|
|
|
|
|
|
|
|
|
Blood, 1 March 2008, Vol. 111, No. 5, pp. 2497-2498.
Mast cells and T-cell expansionNATIONAL RESEARCH INSTITUTE FOR CHILD HEALTH AND DEVELOPMENT
IgE/antigen-Fc
MCs are capable of presenting antigens to T cells by direct cell-cell interaction through antigen-specific T-cell receptor (TCR) and major histocompatibility complex (MHC) class I– or class II–restricted mechanisms in vitro.1 Exosomes released from MCs, which contain MHC class II and antigen complexes, participate in antigen-specific T-cell expansion/activation independently of direct cell-cell contact between T cells and MCs in vitro.1 However, it has remained unclear whether MCs have such functions in vivo.
In the February 1 issue of Blood, Kambayashi and coworkers provided a novel molecular mechanism for MHC class II–restricted, antigen-specific T-cell expansion/activation by murine bone marrow–derived cultured MCs (BMCMCs) in a series of well-designed and elegant experiments. Consistent with prior work,2 they demonstrated that naive BMCMCs showed poor antigen-presenting capabilities to CD4+ T cells from MHC class II–restricted and the ovalbumin (OVA)-specific TCR-transgenic (OTII) stain. However, MHC class II–deficient BMCMCs stimulated in advance with anti-OVA IgE and OVA were found to clearly facilitate OTII T-cell activation without further addition of OVA. In addition, IgE/antigen-Fc
MCs exist in close proximity with T cells in human tonsils3 as well as at the inflammatory sites in mice,2 and in close proximity with DCs in most tissues.4 In addition, MCs can migrate into draining lymph nodes from antigen entry sites.5 Based on the present work by Kambayashi and coworkers, it is possible that IgE/antigen-captured MCs become apoptotic in T-cell zones1 in secondary lymphoid tissues and/or at antigen-challenged inflammatory sites. Thus, DCs can present MC-derived antigens to "antigen-specific," that is, already antigen-sensitized, memory T helper cells. In contrast to a previous report indicating that MC-mediated T-cell activation is Ig/antigen-FcR independent,2 the findings of Kambayashi and colleagues indicate that MC-mediated T-cell activation is dependent on IgE, and thus it cannot be adopted for less/non-IgE–mediated diseases such as autoimmune disorders. Nevertheless, the present findings provide new insight into our understanding of the molecular mechanisms in-volved in the development of IgE- and MC-mediated allergic diseases.
Footnotes
Conflict-of-interest disclosure: H.S. received a grant from the National Institute of Biomedical Innovation. The other authors declare no competing financial interests.
REFERENCES
  CiteULike  Connotea  Del.icio.us  Digg  Reddit  Technorati What's this?
Related Article in Blood Online:
| |||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
 |
 |
 |
|||||||||
 |
 |
 |
 |
 |
 |
 |
 |
||||
| |||||||||||
| Copyright © 2008 by American Society of Hematology Online ISSN: 1528-0020 | |||||||||||
RI crosslinking promotes antigen internalization and apoptosis in mouse mast cells. Dendritic cells uptake the apoptotic mast cells carrying internalized antigens, and thus can efficiently present the antigens to memory T cells. 
