Isolated lymphoid follicles are not IgA inductive sites for recombinant Salmonella
- Department of Microbiology and Immunology, Nihon University School of Dentistry at Matsudo, 2-870-1, Sakaecho-Nishi, Matsudo, Chiba 271-8587 (Japan)
- Department of Food Science and Technology, Nihon University College of Bioresource Sciences, 1866, Kameino, Fujisawa, Kanagawa 252-8510 (Japan)
- Department of Preventive Dentistry, Osaka University Graduate School of Dentistry, 1-8, Yamadaoka, Suita, Osaka 565-0781 (Japan)
- Mucosal Immunology Section, International Vaccine Institute, Seoul National University Research Park, Kwanak-gu, Seoul 151-818, Korea (Korea, Republic of)
In this study, we investigated whether isolated lymphoid follicles (ILF) play a role in the regulation of intestinal IgA antibody (Ab) responses. The transfer of wild type (WT) bone marrow (BM) to lymphotoxin-{alpha}-deficient (LT{alpha}{sup -/-}) mice resulted in the formation of mature ILF containing T cells, B cells, and FDC clusters in the absence of mesenteric lymph nodes and Peyer's patches. Although the ILF restored total IgA Abs in the intestine, antigen (Ag)-specific IgA responses were not induced after oral immunization with recombinant Salmonella expressing fragment C of tetanus toxin. Moreover, Ag-specific cell proliferation was not detected in the ILF. Interestingly, no IgA anti-LPS Abs were detected in the fecal extracts of LT{alpha}{sup -/-} mice reconstituted with WT BM. On the basis of these findings, ILF can be presumed to play a role in the production of IgA Abs, but lymphoid nodules are not inductive sites for the regulation of Ag-specific intestinal IgA responses to recombinant Salmonella.
- OSTI ID:
- 20991503
- Journal Information:
- Biochemical and Biophysical Research Communications, Vol. 360, Issue 2; Other Information: DOI: 10.1016/j.bbrc.2007.06.096; PII: S0006-291X(07)01296-X; Copyright (c) 2007 Elsevier Science B.V., Amsterdam, The Netherlands, All rights reserved; Country of input: International Atomic Energy Agency (IAEA); ISSN 0006-291X
- Country of Publication:
- United States
- Language:
- English
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