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Role of gut-associated lymphoreticular tissues in antigen-specific intestinal IgA immunity. Export

Journal of immunology (Baltimore, Md. : 1950), Vol. 173, No. 2. (15 July 2004), pp. 762-769.

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ilfs lti-cells

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PROTOCOL Treatment of adult mice with LTbR-Ig References IgA regulation 2, 4*,oral immunization of mice that lack PP resulted in the generation of Ag-specific IgA Ab responses in the GI tract (6)/The LT{alpha}{beta} complex binds to a specific receptor termed the LT{beta}R (14)/LT{alpha}{beta} signaling pathway in the intestinal lamina propria is relevant for the production of IgA in a manner shown to be independent of the presence of PP and MLN (26, 27)/ILF formation occurs in small intestine postnatally in response to luminal stimuli, including normal bacterial flora (29, 30) CT-TT oral immunization protocol/ CR1 staining follicular DC marker/

AlfonsoVicenteSuarez (public note) - 2009-11-09 17:50:34

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This study assessed the roles of the postnatal lymphotoxin-beta receptor (LTbetaR)-mediated signals in the gut-associated lymphoreticular tissues of mice for subsequent regulation of Ag-specific intestinal IgA responses. Blockade of LTbetaR-dependent events by postnatal administration of the fusion protein of LTbetaR and IgG Fc (LTbetaR-Ig) reduced both the size and numbers of Peyer's patches (PP) without influencing the PP microarchitecture. Interestingly, inhibition of LTbetaR-dependent signaling revealed significant reductions in the formation of follicular dendritic cell clusters in mesenteric lymph nodes (MLN). Furthermore, these postnatal signaling events controlled the development of isolated lymphoid follicles (ILF) because treatment with LTbetaR-Ig eliminated the formation of ILF. LTbetaR-Ig-treated mice with altered microarchitecture of MLN and lacking ILF were still able to produce significant Ag-specific mucosal IgA responses after oral immunization; however, the levels were significantly lower than those seen in control mice. These results imply the importance of ILF for Ag-specific intestinal immunity. However, mice treated with both TNFR55-Ig and LTbetaR-Ig in utero, which lack PP and MLN, but retain intact ILF, failed to induce Ag-specific IgA responses after oral immunization. These findings demonstrate that ILF are not essential for induction of intestinal IgA Ab responses to orally administered Ag. Furthermore, the induction of intestinal IgA Ab responses requires the proper maintenance of the MLN microarchitecture, including a follicular dendritic cell network.


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