Experimental models to study molecular mechanisms underlying intestinal inflammation

Charles O. Elson; Y. Cong; S. Brandwein; C. T. Weaver; R. P. McCabe; M. Mähler; J. P. Sundberg; E. H. Leiter

doi:10.1111/j.1749-6632.1998.tb11113.x

Experimental models to study molecular mechanisms underlying intestinal inflammation

Charles O. Elson, Y. Cong, S. Brandwein, C. T. Weaver, R. P. McCabe, M. Mähler, J. P. Sundberg, E. H. Leiter

Research output: Contribution to journal › Article › peer-review

78 Scopus citations

Abstract

Experimental animal models, particularly the newer mouse models, have convincingly demonstrated that CD⁺ T cells play a central role in chronic intestinal inflammation. Such CD4⁺ effector T cells are induced by the bacterial flora. In at least one model, it is conventional protein antigens that are stimulating these pathogenic T cells. The antigens driving disease seem to be a selective subset of immunodominant proteins, likely derived from a subset of organisms. Multiple genes contribute to colitis susceptibility and a number of these genes are being localized.

Original language	English (US)
Pages (from-to)	85-95
Number of pages	11
Journal	Annals of the New York Academy of Sciences
Volume	859
DOIs	https://doi.org/10.1111/j.1749-6632.1998.tb11113.x
State	Published - 1998
Externally published	Yes

ASJC Scopus subject areas

General Neuroscience
General Biochemistry, Genetics and Molecular Biology
History and Philosophy of Science

Access to Document

10.1111/j.1749-6632.1998.tb11113.x

Cite this

@article{e302eb05e4ba428da6bd3564b2c49935,

title = "Experimental models to study molecular mechanisms underlying intestinal inflammation",

abstract = "Experimental animal models, particularly the newer mouse models, have convincingly demonstrated that CD+ T cells play a central role in chronic intestinal inflammation. Such CD4+ effector T cells are induced by the bacterial flora. In at least one model, it is conventional protein antigens that are stimulating these pathogenic T cells. The antigens driving disease seem to be a selective subset of immunodominant proteins, likely derived from a subset of organisms. Multiple genes contribute to colitis susceptibility and a number of these genes are being localized.",

author = "Elson, {Charles O.} and Y. Cong and S. Brandwein and Weaver, {C. T.} and McCabe, {R. P.} and M. M{\"a}hler and Sundberg, {J. P.} and Leiter, {E. H.}",

year = "1998",

doi = "10.1111/j.1749-6632.1998.tb11113.x",

language = "English (US)",

volume = "859",

pages = "85--95",

journal = "Annals of the New York Academy of Sciences",

issn = "0077-8923",

publisher = "Wiley-Blackwell",

}

TY - JOUR

T1 - Experimental models to study molecular mechanisms underlying intestinal inflammation

AU - Elson, Charles O.

AU - Cong, Y.

AU - Brandwein, S.

AU - Weaver, C. T.

AU - McCabe, R. P.

AU - Mähler, M.

AU - Sundberg, J. P.

AU - Leiter, E. H.

PY - 1998

Y1 - 1998

N2 - Experimental animal models, particularly the newer mouse models, have convincingly demonstrated that CD+ T cells play a central role in chronic intestinal inflammation. Such CD4+ effector T cells are induced by the bacterial flora. In at least one model, it is conventional protein antigens that are stimulating these pathogenic T cells. The antigens driving disease seem to be a selective subset of immunodominant proteins, likely derived from a subset of organisms. Multiple genes contribute to colitis susceptibility and a number of these genes are being localized.

AB - Experimental animal models, particularly the newer mouse models, have convincingly demonstrated that CD+ T cells play a central role in chronic intestinal inflammation. Such CD4+ effector T cells are induced by the bacterial flora. In at least one model, it is conventional protein antigens that are stimulating these pathogenic T cells. The antigens driving disease seem to be a selective subset of immunodominant proteins, likely derived from a subset of organisms. Multiple genes contribute to colitis susceptibility and a number of these genes are being localized.

UR - http://www.scopus.com/inward/record.url?scp=0032435314&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0032435314&partnerID=8YFLogxK

U2 - 10.1111/j.1749-6632.1998.tb11113.x

DO - 10.1111/j.1749-6632.1998.tb11113.x

M3 - Article

C2 - 9928372

AN - SCOPUS:0032435314

SN - 0077-8923

VL - 859

SP - 85

EP - 95

JO - Annals of the New York Academy of Sciences

JF - Annals of the New York Academy of Sciences

ER -

Experimental models to study molecular mechanisms underlying intestinal inflammation

Abstract

ASJC Scopus subject areas

Access to Document

Other files and links

Fingerprint

Cite this