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Defects of somatic hypermutation and class switching in alymphoplasia (aly) mutant mice
The alymphoplasia (aly) mutation of mice causes the systemic absence of lymph nodes, Peyer's patches and well-defined lymphoid follicles in the spleen. We found that antibody responses are elicited, albelt weakly, to either T cell-dependent or T cell-Independent antigen by aly/aly mutants. Howe...
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Published in: | International immunology 1996-07, Vol.8 (7), p.1067-1075 |
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container_title | International immunology |
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creator | Shinkura, Reiko Matsuda, Fumihiko Sakiyama, Toshio Tsubata, Takeshi Hial, Hiroshi Paumen, Michael Miyawaki, Shigeki Honjo, Tasuku |
description | The alymphoplasia (aly) mutation of mice causes the systemic absence of lymph nodes, Peyer's patches and well-defined lymphoid follicles in the spleen. We found that antibody responses are elicited, albelt weakly, to either T cell-dependent or T cell-Independent antigen by aly/aly mutants. However, isotype switching was defective. The T cell-dependent immune response was not elicited in splenectomized aly/aly mice. Neither hypermutation nor germinal center formation was observed in aly/aly mice. These results suggest that T–B collaboration requires either lymph nodes or spleen, and that hypermutation and affinity maturation depend on germinal center formation. |
doi_str_mv | 10.1093/intimm/8.7.1067 |
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We found that antibody responses are elicited, albelt weakly, to either T cell-dependent or T cell-Independent antigen by aly/aly mutants. However, isotype switching was defective. The T cell-dependent immune response was not elicited in splenectomized aly/aly mice. Neither hypermutation nor germinal center formation was observed in aly/aly mice. These results suggest that T–B collaboration requires either lymph nodes or spleen, and that hypermutation and affinity maturation depend on germinal center formation.</description><identifier>ISSN: 0953-8178</identifier><identifier>EISSN: 1460-2377</identifier><identifier>DOI: 10.1093/intimm/8.7.1067</identifier><identifier>PMID: 8757952</identifier><language>eng</language><publisher>England: Oxford University Press</publisher><subject>aly/aly mice ; Amino Acid Sequence ; Animals ; Antibody Formation - genetics ; Antibody Specificity ; Antigens, T-Independent - physiology ; Base Sequence ; Genetic Variation - genetics ; Genetic Variation - immunology ; Germinal Center - pathology ; immune response ; Immunoglobulin Class Switching ; Immunologic Deficiency Syndromes - genetics ; Immunologic Deficiency Syndromes - pathology ; Lymph Nodes - abnormalities ; Lymphoid Tissue - abnormalities ; Mice ; Mice, Mutant Strains ; Molecular Sequence Data ; Mutation - immunology ; Peyer's Patches - abnormalities ; somatic hypermutation ; Spleen - abnormalities</subject><ispartof>International immunology, 1996-07, Vol.8 (7), p.1067-1075</ispartof><rights>Copyright Oxford University Press(England) Jul 1996</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c555t-5aeed05fe2cd36244a72551b43d6fbd73305448e05d186cecc9fce9b9c9361263</citedby></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,780,784,27924,27925</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/8757952$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Shinkura, Reiko</creatorcontrib><creatorcontrib>Matsuda, Fumihiko</creatorcontrib><creatorcontrib>Sakiyama, Toshio</creatorcontrib><creatorcontrib>Tsubata, Takeshi</creatorcontrib><creatorcontrib>Hial, Hiroshi</creatorcontrib><creatorcontrib>Paumen, Michael</creatorcontrib><creatorcontrib>Miyawaki, Shigeki</creatorcontrib><creatorcontrib>Honjo, Tasuku</creatorcontrib><title>Defects of somatic hypermutation and class switching in alymphoplasia (aly) mutant mice</title><title>International immunology</title><addtitle>Int Immunol</addtitle><description>The alymphoplasia (aly) mutation of mice causes the systemic absence of lymph nodes, Peyer's patches and well-defined lymphoid follicles in the spleen. 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These results suggest that T–B collaboration requires either lymph nodes or spleen, and that hypermutation and affinity maturation depend on germinal center formation.</description><subject>aly/aly mice</subject><subject>Amino Acid Sequence</subject><subject>Animals</subject><subject>Antibody Formation - genetics</subject><subject>Antibody Specificity</subject><subject>Antigens, T-Independent - physiology</subject><subject>Base Sequence</subject><subject>Genetic Variation - genetics</subject><subject>Genetic Variation - immunology</subject><subject>Germinal Center - pathology</subject><subject>immune response</subject><subject>Immunoglobulin Class Switching</subject><subject>Immunologic Deficiency Syndromes - genetics</subject><subject>Immunologic Deficiency Syndromes - pathology</subject><subject>Lymph Nodes - abnormalities</subject><subject>Lymphoid Tissue - abnormalities</subject><subject>Mice</subject><subject>Mice, Mutant Strains</subject><subject>Molecular Sequence Data</subject><subject>Mutation - immunology</subject><subject>Peyer's Patches - abnormalities</subject><subject>somatic hypermutation</subject><subject>Spleen - abnormalities</subject><issn>0953-8178</issn><issn>1460-2377</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>1996</creationdate><recordtype>article</recordtype><recordid>eNqFkb1vFDEQxS0ESo4kNVUkiwJBsbmxvf4qUfgI6BIaUBCN5fN6c07Wu8vaK7j_Hp_ulIIm1ejN-72RRg-hVwQuCGi2DH0OMS7VhSxayGdoQWoBFWVSPkcL0JxVikh1jF6mdA8AjGp2hI6U5FJzukC3H3zrXU54aHEaos3B4c129FOccxFDj23fYNfZlHD6E7LbhP4Oh7LutnHcDGNxgsVvi3yHd5k-4xicP0UvWtslf3aYJ-jHp4_fL6-q1bfPXy7fryrHOc8Vt943wFtPXcMErWsrKedkXbNGtOtGMga8rpUH3hAlnHdOt87rtXaaCUIFO0Fv9nfHafg9-5RNDMn5rrO9H-ZkpKIgBJAnQQpcFZY_CRIuJaEUCvj6P_B-mKe-fGuI5kA0oaxAyz3kpiGlybdmnEK009YQMLsGzb5Bo4w0uwZL4vxwdl5H3zzyh8qKX-39kLL_-2jb6cGUtOTm6ucv8_VGrQiFG3PN_gFI-qb2</recordid><startdate>19960701</startdate><enddate>19960701</enddate><creator>Shinkura, Reiko</creator><creator>Matsuda, Fumihiko</creator><creator>Sakiyama, Toshio</creator><creator>Tsubata, Takeshi</creator><creator>Hial, Hiroshi</creator><creator>Paumen, Michael</creator><creator>Miyawaki, Shigeki</creator><creator>Honjo, Tasuku</creator><general>Oxford University Press</general><general>Oxford Publishing Limited (England)</general><scope>BSCLL</scope><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7QL</scope><scope>7QP</scope><scope>7QR</scope><scope>7T5</scope><scope>7T7</scope><scope>7TK</scope><scope>7U9</scope><scope>8FD</scope><scope>C1K</scope><scope>FR3</scope><scope>H94</scope><scope>K9.</scope><scope>M7N</scope><scope>P64</scope><scope>7X8</scope></search><sort><creationdate>19960701</creationdate><title>Defects of somatic hypermutation and class switching in alymphoplasia (aly) mutant mice</title><author>Shinkura, Reiko ; 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subjects | aly/aly mice Amino Acid Sequence Animals Antibody Formation - genetics Antibody Specificity Antigens, T-Independent - physiology Base Sequence Genetic Variation - genetics Genetic Variation - immunology Germinal Center - pathology immune response Immunoglobulin Class Switching Immunologic Deficiency Syndromes - genetics Immunologic Deficiency Syndromes - pathology Lymph Nodes - abnormalities Lymphoid Tissue - abnormalities Mice Mice, Mutant Strains Molecular Sequence Data Mutation - immunology Peyer's Patches - abnormalities somatic hypermutation Spleen - abnormalities |
title | Defects of somatic hypermutation and class switching in alymphoplasia (aly) mutant mice |
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