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Receptor-Ig Prevents Th2 Cell-Type Colitis1
,
,¶
*
Department of Gastroenterology, Research Institute, International Medical Center of Japan, Tokyo, Japan;
Immunobiology Vaccine Center, Departments of Microbiology and
Oral Biology, University of Alabama, Birmingham, AL 35294;
Biogen, Inc., Cambridge, MA 02142; and
¶ Department of Mucosal Immunology, Research Institute for Microbial Diseases, Osaka University, Osaka, Japan
Past studies have shown that colonic patches, which are the
gut-associated lymphoreticular tissues (GALT) in the colon, become much
more pronounced in hapten-induced murine colitis, and this was
associated with Th2-type T cell responses. To address the role of GALT
in colonic inflammation, experimental colitis was induced in mice
either lacking organized GALT or with altered GALT structures.
Trinitrobenzene sulfonic acid was used to induce colitis in mice given
lymphotoxin-
receptor-Ig fusion protein (LTR-Ig) in utero,
a treatment that blocked the formation of both Peyer’s and colonic
patches. Mice deficient in colonic patches developed focal acute ulcers
with Th1-type responses, whereas lesions in normal mice were of a
diffuse mucosal type with both Th1- and Th2-type cytokine production.
We next determined whether LTR-Ig could be used to treat colitis in
normal or Th2-dominant, IFN-
gene knockout
(IFN--/-) mice. Four weekly treatments with LTR-Ig
resulted in deletion of Peyer’s and colonic patches with significant
decreases in numbers of dendritic cells. This pretreatment protected
IFN--/- mice from trinitrobenzene sulfonic
acid-induced colitis; however, in normal mice this weekly treatment was
less protective. In these mice hypertrophy of colonic patches was seen
after induction of colitis. We conclude that Th2-type colitis is
dependent upon the presence of colonic patches. The effect of LTR-Ig
was mediated through prevention of colonic patch hypertrophy in the
absence of IFN-. Thus, LTR-Ig may offer a possible treatment for
the Th2-dominant form of colitis.
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