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Expression
of Costimulatory Molecules B7-1 and B7-2 in Macrophages and Granulomas of
Crohn's Disease: Demonstration of Cell-to-Cell Contact with T Lymphocytes |
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Junichi Hara,
Haruo Ohtani, Takayuki Matsumoto, Shiro Nakamura, Atsuo Kitano, Tetsuo Arakawa,
Hiroshi Nagura, and Kenzo Kobayashi |
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Department
of Internal Medicine (JH, TM, SN, TA, KK), Osaka City University Medical
School, and Department of Internal Medicine (AK), Juso Municipal Hospital,
Osaka; and Department of Pathology (HO, HN), Tohoku University School of
Medicine, Sendai, Japan |
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The pathogenesis of Crohn's
disease, an intractable inflammatory disease, involves impaired and/or excessive
activation of mucosal macrophages and T lymphocytes. B7-1 (CD80) and B7-2
(CD86) molecules are costimulatory molecules that are indispensable to T-cell
activation by antigen-presenting cells. To elucidate the roles and characteristics
of these antigen-presenting cells in Crohn's disease, in situ localization
of B7-1 and B7-2 (in relation to the distribution of T cells) was clarified
by light and electron microscopic immunohistochemistry. The results were
compared with those from a study of ulcerative colitis. Normal colonic tissue
expressed B7-1 or B7-2 only sporadically. In active Crohn's disease, however,
an increase in the number of B7-1/B7-2+ cells correlated with an increase
in expression of HLA-DR and intercellular adhesion molecule-1. Most B7-1/B7-2+
cells were identified as noncaseating granulomas or as macrophages, which
tended to form an aggregate especially in ulcer bases. In active ulcerative
colitis, the increase of B7-1/B7-2+ cells was not as prominent as that in
Crohn's disease. Double immunohistochemistry revealed a close cellular distribution
between noncaseating granulomas and T cells. Immunoelectron microscopy confirmed
the expression of B7-1/B7-2 along the plasma membranes of cytoplasmic processes
of granuloma cells, where lymphocytes were closely attached. The present
study suggested that granuloma formation in Crohn's disease is coupled with
antigen presentation via a B7-1/B7-2-CD28 pathway, which may contribute
to the pathogenesis of the disease. |
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