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Receptor and TNF Receptor p55 Signaling Cascade Resulted in the Acceleration of Tissue Genesis for Isolated Lymphoid Follicles in the Large Intestine1
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* Mucosal Immunology Section, International Vaccine Institute, Seoul, Korea;
Division of Mucosal Immunology, Institute of Medical Science, University of Tokyo, Tokyo, Japan;
Department of Oral Medicine, Nihon University School of Dentistry at Masudo, Matsudo, Chiba, Japan;
Department of Immunology and Inflammation, Biogen-Idec, Cambridge, MA 02142;
¶ Yakult Central Institute for Microbiological Research, Tokyo, Japan; and
|| Core Research for Engineering, Science, and Technology, Japan Science Technology, Tokyo, Japan
Signaling by lymphotoxin (LT) and TNF is essential for the organogenesis of secondary lymphoid tissues in systemic and mucosal compartments. In this study, we demonstrated that the progeny of mice treated with fusion protein of LT
R and IgGFc (LTR-Ig) or LTR-Ig plus TNFR55-Ig (double Ig) showed significantly increased numbers of isolated lymphoid follicles (ILF) in the large intestine. Interestingly, double Ig treatment accelerated the maturation of large intestinal ILF. Three-week-old progeny of double Ig-treated mice showed increased numbers of ILF in the large intestine, but not in the small intestine. Furthermore, alteration of intestinal microflora by feeding of antibiotic water did not affect the increased numbers of ILF in the large intestine of double Ig-treated mice. Most interestingly, mice that developed numerous ILF also had increased levels of activation-induced cytidine deaminase expression and numbers of IgA-expressing cells in the lamina propria of the large intestine. Taken together, these results suggest that ILF formation in the large intestine is accelerated by blockage of LTR and TNFR55 signals in utero, and ILF, like colonic patches, might play a role in the induction of IgA response in the large intestine.
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