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Journal Article | Research Support, Non-U.S. Gov't

Potential role of molecular mimicry between Helicobacter pylori lipopolysaccharide and host Lewis blood group antigens in autoimmunity.

B J Appelmelk, I Simoons-Smit, R Negrini, A P Moran, G O Aspinall, J G Forte, T De Vries, H Quan, T Verboom, J J Maaskant, P Ghiara, E J Kuipers, E Bloemena, T M Tadema, R R Townsend, K Tyagarajan, J M Crothers Jr, M A Monteiro, A Savio, J De Graaff
B J Appelmelk
Department of Medical Microbiology, Vrije Universiteit Medical School and Academic Hospital, Amsterdam, The Netherlands.
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I Simoons-Smit
Department of Medical Microbiology, Vrije Universiteit Medical School and Academic Hospital, Amsterdam, The Netherlands.
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R Negrini
Department of Medical Microbiology, Vrije Universiteit Medical School and Academic Hospital, Amsterdam, The Netherlands.
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A P Moran
Department of Medical Microbiology, Vrije Universiteit Medical School and Academic Hospital, Amsterdam, The Netherlands.
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G O Aspinall
Department of Medical Microbiology, Vrije Universiteit Medical School and Academic Hospital, Amsterdam, The Netherlands.
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J G Forte
Department of Medical Microbiology, Vrije Universiteit Medical School and Academic Hospital, Amsterdam, The Netherlands.
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T De Vries
Department of Medical Microbiology, Vrije Universiteit Medical School and Academic Hospital, Amsterdam, The Netherlands.
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H Quan
Department of Medical Microbiology, Vrije Universiteit Medical School and Academic Hospital, Amsterdam, The Netherlands.
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T Verboom
Department of Medical Microbiology, Vrije Universiteit Medical School and Academic Hospital, Amsterdam, The Netherlands.
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J J Maaskant
Department of Medical Microbiology, Vrije Universiteit Medical School and Academic Hospital, Amsterdam, The Netherlands.
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P Ghiara
Department of Medical Microbiology, Vrije Universiteit Medical School and Academic Hospital, Amsterdam, The Netherlands.
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E J Kuipers
Department of Medical Microbiology, Vrije Universiteit Medical School and Academic Hospital, Amsterdam, The Netherlands.
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E Bloemena
Department of Medical Microbiology, Vrije Universiteit Medical School and Academic Hospital, Amsterdam, The Netherlands.
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T M Tadema
Department of Medical Microbiology, Vrije Universiteit Medical School and Academic Hospital, Amsterdam, The Netherlands.
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R R Townsend
Department of Medical Microbiology, Vrije Universiteit Medical School and Academic Hospital, Amsterdam, The Netherlands.
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K Tyagarajan
Department of Medical Microbiology, Vrije Universiteit Medical School and Academic Hospital, Amsterdam, The Netherlands.
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J M Crothers Jr
Department of Medical Microbiology, Vrije Universiteit Medical School and Academic Hospital, Amsterdam, The Netherlands.
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M A Monteiro
Department of Medical Microbiology, Vrije Universiteit Medical School and Academic Hospital, Amsterdam, The Netherlands.
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A Savio
Department of Medical Microbiology, Vrije Universiteit Medical School and Academic Hospital, Amsterdam, The Netherlands.
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J De Graaff
Department of Medical Microbiology, Vrije Universiteit Medical School and Academic Hospital, Amsterdam, The Netherlands.
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DOI: 
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ABSTRACT

Helicobacter pylori is involved in gastritis, gastric and duodenal ulcers, gastric adenocarcinoma, and mucosa-associated lymphoid tissue lymphoma. Earlier studies already suggested a role for autoimmune phenomena in H. pylori-linked disease. We now report that lipopolysaccharides (LPS) of H. pylori express Lewis y, Lewis x, and H type I blood group structures similar to those commonly occurring in gastric mucosa. Immunization of mice and rabbits with H. pylori cells or purified LPS induced an anti-Lewis x or y or anti-H type I response, yielding antibodies that bound human and murine gastric glandular tissue, granulocytes, adenocarcinoma, and mucosa-associated lymphoid tissue lymphoma cells. Experimental oral infections in mice or natural infection in humans yielded anti-Lewis antibodies also. The beta chain of gastric (H+,K+)-ATPase, the parietal cell proton pump involved in acid secretion, contained Lewis y epitopes; gastric mucin contained Lewis x and y antigenic determinants. Growth in mice of a hybridoma that secretes H. pylori-induced anti-Lewis y monoclonal antibodies resulted in histopathological evidence of gastritis, which indicates a direct pathogenic role for anti-Lewis antibodies. In conclusion, our observations demonstrate that molecular mimicry between H. pylori LPS and the host, based on Lewis antigens, and provide understanding of an autoimmune mechanism for H. pylori-associated type B gastritis.

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Potential role of molecular mimicry between Helicobacter pylori lipopolysaccharide and host Lewis blood group antigens in autoimmunity.
B J Appelmelk, I Simoons-Smit, R Negrini, A P Moran, G O Aspinall, J G Forte, T De Vries, H Quan, T Verboom, J J Maaskant, P Ghiara, E J Kuipers, E Bloemena, T M Tadema, R R Townsend, K Tyagarajan, J M Crothers Jr, M A Monteiro, A Savio, J De Graaff
Infection and Immunity Jun 1996, 64 (6) 2031-2040; DOI:

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Potential role of molecular mimicry between Helicobacter pylori lipopolysaccharide and host Lewis blood group antigens in autoimmunity.
B J Appelmelk, I Simoons-Smit, R Negrini, A P Moran, G O Aspinall, J G Forte, T De Vries, H Quan, T Verboom, J J Maaskant, P Ghiara, E J Kuipers, E Bloemena, T M Tadema, R R Townsend, K Tyagarajan, J M Crothers Jr, M A Monteiro, A Savio, J De Graaff
Infection and Immunity Jun 1996, 64 (6) 2031-2040; DOI:
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