Genetic and environmental context determines the course of colitis developing in IL-10-deficient mice.

Abstract:

:This review summarizes how interleukin-10 (IL-10)-deficient mice have permitted new insight into the complex interaction between genes and environment underlying pathogenesis of inflammatory bowel disease (IBD). The C57BL/6J strain develops only mild typhlocolitis in response to IL-10 deficiency. In contrast, C3H/HeJBir represents an unrelated inbred strain with high IBD susceptibility. Ability to identify quantitative trait loci segregating for susceptibility when the two IL-10-deficient stocks were intercrossed depended both on genome "context" (F2 versus reciprocal backcrosses) and on the physical environment. These findings are discussed in the context of recent advances in understanding the complex genetic basis for IBD in humans.

journal_name

Inflamm Bowel Dis

authors

Mähler M,Leiter EH

doi

10.1097/00054725-200209000-00006

keywords:

subject

Has Abstract

pub_date

2002-09-01 00:00:00

pages

347-55

issue

5

eissn

1078-0998

issn

1536-4844

journal_volume

8

pub_type

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