Diseases caused by reactions of T lymphocytes towards incompatible structures of the major histocompatibility complex. VI. Autoantibodies characteristic of systemic lupus erythematosus induced by abnormal T-B cell cooperation across I-E

doi:10.1084/jem.155.5.1555

This Article

	Full Text (PDF, 374K)
	Alert me when this article is cited
	Citation Map

Services

	Email this article
	Similar articles in this journal
	Similar articles in PubMed
	Alert me to new content in the JEM
	Download to citation manager

Citing Articles

	Citing Articles via HighWire
	Citing Articles via CrossRef
	Citing Articles via Google Scholar

Google Scholar

	Articles by van Rappard-van der Veen, F. M.
	Articles by Gleichmann, E.
	Search for Related Content

PubMed

	PubMed Citation
	Articles by van Rappard-van der Veen, F. M.
	Articles by Gleichmann, E.


Social Bookmarking

	What's this?

ARTICLES

Diseases caused by reactions of T lymphocytes towards incompatible structures of the major histocompatibility complex. VI. Autoantibodies characteristic of systemic lupus erythematosus induced by abnormal T-B cell cooperation across I-E

FM van Rappard-van der Veen, AG Rolink and E Gleichmann

By induction of a suitable graft-vs-host reaction (GVHR) in H-2- different F1 mice, one can induce the production of autoantibodies characteristic of systemic lupus erythematosus (SLE). The purpose of the present study was to define the intra-H-2 differences in the F1 recipients that are capable of triggering this process. A GVHR was induced in [B10.A(2R) x B10.A(4R)]F1 mice by injecting 10(8) lymphocytes from either parental strain. Whereas the donor B10.A(4R) induced a massive formation of autoantibodies to thymocytes, erythrocytes, nuclear antigens, and double-stranded DNA, the donor B10.A(2R) failed to do so. The intra-H-2 genetics of these two parent leads to F1 combinations are such that the observed autoantibody formation after the injection of B10.A(4R) T cells must have been triggered exclusively by the incompatible I-Ek subregion of the [B10.A(2R) x B10.A(4R)]F1 recipients. Because I-E appears to be the murine analogue of HLA-D/DR, this finding is of interest with respect to the increased frequency of certain HLA-DR alleles in SLE patients, as discussed.
Add to CiteULike CiteULike Add to Complore Complore Add to Connotea Connotea Add to Del.icio.us Del.icio.us Add to Digg Digg Facebook Add to Reddit Reddit Add to Technorati Technorati Twitter What's this?

This article has been cited by other articles:

Giorgini, A., Noble, A. (2007). Blockade of chronic graft-versus-host disease by alloantigen-induced CD4+CD25+Foxp3+ regulatory T cells in nonlymphopenic hosts. J. Leukoc. Biol. 82: 1053-1061 [Abstract] [Full Text]
Grader-Beck, T., Casciola-Rosen, L., Lang, T. J., Puliaev, R., Rosen, A., Via, C. S. (2007). Apoptotic Splenocytes Drive the Autoimmune Response to Poly(ADP-ribose) Polymerase 1 in a Murine Model of Lupus. J. Immunol. 178: 95-102 [Abstract] [Full Text]
Witsch, E. J., Cao, H., Fukuyama, H., Weigert, M. (2006). Light chain editing generates polyreactive antibodies in chronic graft-versus-host reaction. JEM 203: 1761-1772 [Abstract] [Full Text]
Choudhury, A., Maldonado, M. A., Cohen, P. L., Eisenberg, R. A. (2005). The Role of Host CD4 T Cells in the Pathogenesis of the Chronic Graft-versus-Host Model of Systemic Lupus Erythematosus. J. Immunol. 174: 7600-7609 [Abstract] [Full Text]
Sekiguchi, D. R., Eisenberg, R. A., Weigert, M. (2003). Secondary Heavy Chain Rearrangement: A Mechanism for Generating Anti-double-stranded DNA B Cells. JEM 197: 27-39 [Abstract] [Full Text]
Sekiguchi, D. R., Jainandunsing, S. M., Fields, M. L., Maldonado, M. A., Madaio, M. P., Erikson, J., Weigert, M., Eisenberg, R. A. (2002). Chronic Graft-Versus-Host in Ig Knockin Transgenic Mice Abrogates B Cell Tolerance in Anti-Double-Stranded DNA B Cells. J. Immunol. 168: 4142-4153 [Abstract] [Full Text]
Laufer, T. M., Fan, L., Glimcher, L. H. (1999). Self-Reactive T Cells Selected on Thymic Cortical Epithelium Are Polyclonal and Are Pathogenic In Vivo. J. Immunol. 162: 5078-5084 [Abstract] [Full Text]