Literature DB >> 3576135

Protection against cholera toxin after oral immunization is thymus-dependent and associated with intestinal production of neutralizing IgA antitoxin.

N Lycke, L Eriksen, J Holmgren.   

Abstract

We studied whether gut mucosal IgA antitoxin production as well as the acquired protection against cholera toxin (CT) after oral immunization with CT are both thymus-dependent immune manifestations. In contrast to normal BALB/c mice, nude, athymic mice did not respond to oral immunizations with CT with either IgA antitoxin-producing cells (SFC) in the lamina propria or protection against challenge with CT in ligated intestinal loops. However, when nude mice were first reconstituted by grafting of syngeneic thymus glands, both IgA antitoxin SFC in the lamina propria and protection were stimulated by oral immunizations with CT and the response were of similar magnitude to those of normal mice after immunizations. During in vitro culture, isolated lamina propria lymphocytes from immunized but not from control mice concomitantly and proportionally produced IgA antitoxin and CT-neutralizing activity. We conclude that intestinal antitoxin formation and protection against toxin challenge after oral immunization with CT are both critically thymus-dependent and therefore likely to be under T-cell control.

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Year:  1987        PMID: 3576135     DOI: 10.1111/j.1365-3083.1987.tb02208.x

Source DB:  PubMed          Journal:  Scand J Immunol        ISSN: 0300-9475            Impact factor:   3.487


  23 in total

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8.  Deficient induction of the immune response to oral immunization with cholera toxin in malnourished rats during suckling.

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9.  A T cell-dependent mechanism for the induction of human mucosal homing immunoglobulin A-secreting plasmablasts.

Authors:  Melissa Dullaers; Dapeng Li; Yaming Xue; Ling Ni; Ingrid Gayet; Rimpei Morita; Hideki Ueno; Karolina Anna Palucka; Jacques Banchereau; Sangkon Oh
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10.  Analysis of the roles of antilipopolysaccharide and anti-cholera toxin immunoglobulin A (IgA) antibodies in protection against Vibrio cholerae and cholera toxin by use of monoclonal IgA antibodies in vivo.

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