Evidence for a selected humoral immune response encoded by VH4 family genes in the synovial membrane of a patient with rheumatoid arthritis (RA)
Identifieur interne : 001214 ( PascalFrancis/Checkpoint ); précédent : 001213; suivant : 001215Evidence for a selected humoral immune response encoded by VH4 family genes in the synovial membrane of a patient with rheumatoid arthritis (RA)
Auteurs : J. Voswinkel [Allemagne] ; L. Trümper [Allemagne] ; G. Carbon [Allemagne] ; T. Hopf [Allemagne] ; M. Pfreundschuh [Allemagne] ; A. Gause [Allemagne]Source :
- Clinical and experimental immunology [ 0009-9104 ] ; 1996.
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Abstract
The analysis of rearranged antibody-encoding genes from B cell foci in rheumatoid synovial tissue has characterized these cells as highly mutated memory B cells with a high proportion of members of the VH4 family. In order to characterize further the VH4 response in one patient, B cell-rich areas from different sections of synovial membrane (SM) were identified by CD20 staining, isolated by microdissection and pooled in order to analyse highly enriched B cells without selection by in vitro culture procedures. From DNA of about 5 x 103 B cells rearranged VH genes were amplified by polymerase chain reaction (PCR) and cloned. Sequencing of 11 clones containing rearranged VH4 gene products revealed that seven were potentially functional, and all were mutated with 84-96% homology to known germ-line (gl) genes and VH4 gl genes amplified from the patient's genomic DNA. Analysis of the complementarity determining region (CDR) 3 revealed that two products represented members of one B cell clone which differed by five nucleotide changes. Three of the five mutations encoded amino acid replacements in CDRs indicating antigen-driven expansion of one specific clone. Additional analyses of 25 members of three B cell clones from isolated aggregates showing intraclonal diversity in one of three clones provided further evidence that antigen selection takes place in the SM. Overall, the pattern of mutations and the replacement to silent (R:S) ratios were diverse, with six products indicating antigen selection by their high R:S ratios in CDRs. Although DNA analysis does not allow a characterization of antibody specificities, we can conclude from our analysis of antibody-encoding genes that selection by antigen and expansion of specific clones occur in the SM against the background of polyclonal activation.
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Voswinkel</name><affiliation wicri:level="1"><inist:fA14 i1="01"><s1>Internal Medicine I, Saarland Medical School</s1><s2>Homburg/Saar</s2><s3>DEU</s3><sZ>1 aut.</sZ><sZ>2 aut.</sZ><sZ>3 aut.</sZ><sZ>5 aut.</sZ><sZ>6 aut.</sZ></inist:fA14><country>Allemagne</country><wicri:noRegion>Homburg/Saar</wicri:noRegion><wicri:noRegion>Saarland Medical School</wicri:noRegion><wicri:noRegion>Homburg/Saar</wicri:noRegion></affiliation></author><author><name sortKey="Trumper, L" sort="Trumper, L" uniqKey="Trumper L" first="L." last="Trümper">L. Trümper</name><affiliation wicri:level="1"><inist:fA14 i1="01"><s1>Internal Medicine I, Saarland Medical School</s1><s2>Homburg/Saar</s2><s3>DEU</s3><sZ>1 aut.</sZ><sZ>2 aut.</sZ><sZ>3 aut.</sZ><sZ>5 aut.</sZ><sZ>6 aut.</sZ></inist:fA14><country>Allemagne</country><wicri:noRegion>Homburg/Saar</wicri:noRegion><wicri:noRegion>Saarland Medical School</wicri:noRegion><wicri:noRegion>Homburg/Saar</wicri:noRegion></affiliation></author><author><name sortKey="Carbon, G" sort="Carbon, G" uniqKey="Carbon G" first="G." last="Carbon">G. Carbon</name><affiliation wicri:level="1"><inist:fA14 i1="01"><s1>Internal Medicine I, Saarland Medical School</s1><s2>Homburg/Saar</s2><s3>DEU</s3><sZ>1 aut.</sZ><sZ>2 aut.</sZ><sZ>3 aut.</sZ><sZ>5 aut.</sZ><sZ>6 aut.</sZ></inist:fA14><country>Allemagne</country><wicri:noRegion>Homburg/Saar</wicri:noRegion><wicri:noRegion>Saarland Medical School</wicri:noRegion><wicri:noRegion>Homburg/Saar</wicri:noRegion></affiliation></author><author><name sortKey="Hopf, T" sort="Hopf, T" uniqKey="Hopf T" first="T." last="Hopf">T. Hopf</name><affiliation wicri:level="1"><inist:fA14 i1="02"><s1>Department of Orthopaedics, Krankenhaus der Barmherzigen Brüder</s1><s2>Trier</s2><s3>DEU</s3><sZ>4 aut.</sZ></inist:fA14><country>Allemagne</country><wicri:noRegion>Trier</wicri:noRegion><wicri:noRegion>Krankenhaus der Barmherzigen Brüder</wicri:noRegion><wicri:noRegion>Trier</wicri:noRegion></affiliation></author><author><name sortKey="Pfreundschuh, M" sort="Pfreundschuh, M" uniqKey="Pfreundschuh M" first="M." last="Pfreundschuh">M. Pfreundschuh</name><affiliation wicri:level="1"><inist:fA14 i1="01"><s1>Internal Medicine I, Saarland Medical School</s1><s2>Homburg/Saar</s2><s3>DEU</s3><sZ>1 aut.</sZ><sZ>2 aut.</sZ><sZ>3 aut.</sZ><sZ>5 aut.</sZ><sZ>6 aut.</sZ></inist:fA14><country>Allemagne</country><wicri:noRegion>Homburg/Saar</wicri:noRegion><wicri:noRegion>Saarland Medical School</wicri:noRegion><wicri:noRegion>Homburg/Saar</wicri:noRegion></affiliation></author><author><name sortKey="Gause, A" sort="Gause, A" uniqKey="Gause A" first="A." last="Gause">A. Gause</name><affiliation wicri:level="1"><inist:fA14 i1="01"><s1>Internal Medicine I, Saarland Medical School</s1><s2>Homburg/Saar</s2><s3>DEU</s3><sZ>1 aut.</sZ><sZ>2 aut.</sZ><sZ>3 aut.</sZ><sZ>5 aut.</sZ><sZ>6 aut.</sZ></inist:fA14><country>Allemagne</country><wicri:noRegion>Homburg/Saar</wicri:noRegion><wicri:noRegion>Saarland Medical School</wicri:noRegion><wicri:noRegion>Homburg/Saar</wicri:noRegion></affiliation></author></analytic><series><title level="j" type="main">Clinical and experimental immunology</title><title level="j" type="abbreviated">Clin. exp. immunol.</title><idno type="ISSN">0009-9104</idno><imprint><date when="1996">1996</date></imprint></series></biblStruct></sourceDesc><seriesStmt><title level="j" type="main">Clinical and experimental immunology</title><title level="j" type="abbreviated">Clin. exp. immunol.</title><idno type="ISSN">0009-9104</idno></seriesStmt></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Adhesion</term><term>B-Lymphocyte</term><term>Cell adhesion molecule</term><term>Chronic</term><term>Cytokine</term><term>Genetics</term><term>Human</term><term>Humoral immunity</term><term>Immune response</term><term>Immunological investigation</term><term>Integrin</term><term>Monocyte</term><term>Rheumatoid arthritis</term><term>Somatic mutation</term><term>Synovial membrane</term><term>Synovitis</term></keywords><keywords scheme="Pascal" xml:lang="fr"><term>Polyarthrite rhumatoïde</term><term>Adhérence</term><term>Génétique</term><term>Intégrine</term><term>Homme</term><term>Protéine CAM</term><term>Cytokine</term><term>Monocyte</term><term>Synovite</term><term>Réponse immune</term><term>Immunité humorale</term><term>Mutation somatique</term><term>Exploration immunologique</term><term>Lymphocyte B</term><term>Synoviale</term><term>Chronique</term></keywords><keywords scheme="Wicri" type="topic" xml:lang="fr"><term>Génétique</term><term>Homme</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">The analysis of rearranged antibody-encoding genes from B cell foci in rheumatoid synovial tissue has characterized these cells as highly mutated memory B cells with a high proportion of members of the V<sub>H</sub>4 family. In order to characterize further the V<sub>H</sub>4 response in one patient, B cell-rich areas from different sections of synovial membrane (SM) were identified by CD20 staining, isolated by microdissection and pooled in order to analyse highly enriched B cells without selection by in vitro culture procedures. From DNA of about 5 x 10<sup>3</sup> B cells rearranged V<sub>H</sub> genes were amplified by polymerase chain reaction (PCR) and cloned. Sequencing of 11 clones containing rearranged V<sub>H</sub>4 gene products revealed that seven were potentially functional, and all were mutated with 84-96% homology to known germ-line (gl) genes and V<sub>H</sub>4 gl genes amplified from the patient's genomic DNA. Analysis of the complementarity determining region (CDR) 3 revealed that two products represented members of one B cell clone which differed by five nucleotide changes. Three of the five mutations encoded amino acid replacements in CDRs indicating antigen-driven expansion of one specific clone. Additional analyses of 25 members of three B cell clones from isolated aggregates showing intraclonal diversity in one of three clones provided further evidence that antigen selection takes place in the SM. Overall, the pattern of mutations and the replacement to silent (R:S) ratios were diverse, with six products indicating antigen selection by their high R:S ratios in CDRs. Although DNA analysis does not allow a characterization of antibody specificities, we can conclude from our analysis of antibody-encoding genes that selection by antigen and expansion of specific clones occur in the SM against the background of polyclonal activation.</div></front></TEI><inist><standard h6="B"><pA><fA01 i1="01" i2="1"><s0>0009-9104</s0></fA01><fA02 i1="01"><s0>CEXIAL</s0></fA02><fA03 i2="1"><s0>Clin. exp. immunol.</s0></fA03><fA05><s2>106</s2></fA05><fA06><s2>1</s2></fA06><fA08 i1="01" i2="1" l="ENG"><s1>Evidence for a selected humoral immune response encoded by V<sub>H</sub>4 family genes in the synovial membrane of a patient with rheumatoid arthritis (RA)</s1></fA08><fA11 i1="01" i2="1"><s1>VOSWINKEL (J.)</s1></fA11><fA11 i1="02" i2="1"><s1>TRÜMPER (L.)</s1></fA11><fA11 i1="03" i2="1"><s1>CARBON (G.)</s1></fA11><fA11 i1="04" i2="1"><s1>HOPF (T.)</s1></fA11><fA11 i1="05" i2="1"><s1>PFREUNDSCHUH (M.)</s1></fA11><fA11 i1="06" i2="1"><s1>GAUSE (A.)</s1></fA11><fA14 i1="01"><s1>Internal Medicine I, Saarland Medical School</s1><s2>Homburg/Saar</s2><s3>DEU</s3><sZ>1 aut.</sZ><sZ>2 aut.</sZ><sZ>3 aut.</sZ><sZ>5 aut.</sZ><sZ>6 aut.</sZ></fA14><fA14 i1="02"><s1>Department of Orthopaedics, Krankenhaus der Barmherzigen Brüder</s1><s2>Trier</s2><s3>DEU</s3><sZ>4 aut.</sZ></fA14><fA20><s1>5-12</s1></fA20><fA21><s1>1996</s1></fA21><fA23 i1="01"><s0>ENG</s0></fA23><fA43 i1="01"><s1>INIST</s1><s2>12690</s2><s5>354000063024350020</s5></fA43><fA44><s0>0000</s0><s1>© 1997 INIST-CNRS. All rights reserved.</s1></fA44><fA45><s0>40 ref.</s0></fA45><fA47 i1="01" i2="1"><s0>97-0170603</s0></fA47><fA60><s1>P</s1></fA60><fA61><s0>A</s0></fA61><fA64 i1="01" i2="1"><s0>Clinical and experimental immunology</s0></fA64><fA66 i1="01"><s0>GBR</s0></fA66><fC01 i1="01" l="ENG"><s0>The analysis of rearranged antibody-encoding genes from B cell foci in rheumatoid synovial tissue has characterized these cells as highly mutated memory B cells with a high proportion of members of the V<sub>H</sub>4 family. In order to characterize further the V<sub>H</sub>4 response in one patient, B cell-rich areas from different sections of synovial membrane (SM) were identified by CD20 staining, isolated by microdissection and pooled in order to analyse highly enriched B cells without selection by in vitro culture procedures. From DNA of about 5 x 10<sup>3</sup> B cells rearranged V<sub>H</sub> genes were amplified by polymerase chain reaction (PCR) and cloned. Sequencing of 11 clones containing rearranged V<sub>H</sub>4 gene products revealed that seven were potentially functional, and all were mutated with 84-96% homology to known germ-line (gl) genes and V<sub>H</sub>4 gl genes amplified from the patient's genomic DNA. Analysis of the complementarity determining region (CDR) 3 revealed that two products represented members of one B cell clone which differed by five nucleotide changes. Three of the five mutations encoded amino acid replacements in CDRs indicating antigen-driven expansion of one specific clone. Additional analyses of 25 members of three B cell clones from isolated aggregates showing intraclonal diversity in one of three clones provided further evidence that antigen selection takes place in the SM. Overall, the pattern of mutations and the replacement to silent (R:S) ratios were diverse, with six products indicating antigen selection by their high R:S ratios in CDRs. Although DNA analysis does not allow a characterization of antibody specificities, we can conclude from our analysis of antibody-encoding genes that selection by antigen and expansion of specific clones occur in the SM against the background of polyclonal activation.</s0></fC01><fC02 i1="01" i2="X"><s0>002B15D</s0></fC02><fC03 i1="01" i2="X" l="FRE"><s0>Polyarthrite rhumatoïde</s0><s5>01</s5></fC03><fC03 i1="01" i2="X" l="ENG"><s0>Rheumatoid arthritis</s0><s5>01</s5></fC03><fC03 i1="01" i2="X" l="SPA"><s0>Poliartritis reumatoidea</s0><s5>01</s5></fC03><fC03 i1="02" i2="X" l="FRE"><s0>Adhérence</s0><s5>02</s5></fC03><fC03 i1="02" i2="X" l="ENG"><s0>Adhesion</s0><s5>02</s5></fC03><fC03 i1="02" i2="X" l="GER"><s0>Adhaesion</s0><s5>02</s5></fC03><fC03 i1="02" i2="X" l="SPA"><s0>Adherencia</s0><s5>02</s5></fC03><fC03 i1="03" i2="X" l="FRE"><s0>Génétique</s0><s5>03</s5></fC03><fC03 i1="03" i2="X" l="ENG"><s0>Genetics</s0><s5>03</s5></fC03><fC03 i1="03" i2="X" l="SPA"><s0>Genética</s0><s5>03</s5></fC03><fC03 i1="04" i2="X" l="FRE"><s0>Intégrine</s0><s5>04</s5></fC03><fC03 i1="04" i2="X" l="ENG"><s0>Integrin</s0><s5>04</s5></fC03><fC03 i1="04" i2="X" l="SPA"><s0>Integrina</s0><s5>04</s5></fC03><fC03 i1="05" i2="X" l="FRE"><s0>Homme</s0><s5>05</s5></fC03><fC03 i1="05" i2="X" l="ENG"><s0>Human</s0><s5>05</s5></fC03><fC03 i1="05" i2="X" l="SPA"><s0>Hombre</s0><s5>05</s5></fC03><fC03 i1="06" i2="X" l="FRE"><s0>Protéine CAM</s0><s5>06</s5></fC03><fC03 i1="06" i2="X" l="ENG"><s0>Cell adhesion molecule</s0><s5>06</s5></fC03><fC03 i1="06" i2="X" l="SPA"><s0>Proteína CAM</s0><s5>06</s5></fC03><fC03 i1="07" i2="X" l="FRE"><s0>Cytokine</s0><s5>07</s5></fC03><fC03 i1="07" i2="X" l="ENG"><s0>Cytokine</s0><s5>07</s5></fC03><fC03 i1="07" i2="X" l="SPA"><s0>Citoquina</s0><s5>07</s5></fC03><fC03 i1="08" i2="X" l="FRE"><s0>Monocyte</s0><s5>08</s5></fC03><fC03 i1="08" i2="X" l="ENG"><s0>Monocyte</s0><s5>08</s5></fC03><fC03 i1="08" i2="X" l="SPA"><s0>Monocito</s0><s5>08</s5></fC03><fC03 i1="09" i2="X" l="FRE"><s0>Synovite</s0><s5>10</s5></fC03><fC03 i1="09" i2="X" l="ENG"><s0>Synovitis</s0><s5>10</s5></fC03><fC03 i1="09" i2="X" l="SPA"><s0>Sinovitis</s0><s5>10</s5></fC03><fC03 i1="10" i2="X" l="FRE"><s0>Réponse immune</s0><s5>11</s5></fC03><fC03 i1="10" i2="X" l="ENG"><s0>Immune response</s0><s5>11</s5></fC03><fC03 i1="10" i2="X" l="SPA"><s0>Respuesta inmune</s0><s5>11</s5></fC03><fC03 i1="11" i2="X" l="FRE"><s0>Immunité humorale</s0><s5>12</s5></fC03><fC03 i1="11" i2="X" l="ENG"><s0>Humoral immunity</s0><s5>12</s5></fC03><fC03 i1="11" i2="X" l="SPA"><s0>Inmunidad humoral</s0><s5>12</s5></fC03><fC03 i1="12" i2="X" l="FRE"><s0>Mutation somatique</s0><s5>13</s5></fC03><fC03 i1="12" i2="X" l="ENG"><s0>Somatic mutation</s0><s5>13</s5></fC03><fC03 i1="12" i2="X" l="SPA"><s0>Mutación somática</s0><s5>13</s5></fC03><fC03 i1="13" i2="X" l="FRE"><s0>Exploration immunologique</s0><s5>19</s5></fC03><fC03 i1="13" i2="X" l="ENG"><s0>Immunological investigation</s0><s5>19</s5></fC03><fC03 i1="13" i2="X" l="SPA"><s0>Análisis inmunológico</s0><s5>19</s5></fC03><fC03 i1="14" i2="X" l="FRE"><s0>Lymphocyte B</s0><s5>20</s5></fC03><fC03 i1="14" i2="X" l="ENG"><s0>B-Lymphocyte</s0><s5>20</s5><s6>«B»-Lymphocyte</s6></fC03><fC03 i1="14" i2="X" l="SPA"><s0>Linfocito B</s0><s5>20</s5></fC03><fC03 i1="15" i2="X" l="FRE"><s0>Synoviale</s0><s5>21</s5></fC03><fC03 i1="15" i2="X" l="ENG"><s0>Synovial membrane</s0><s5>21</s5></fC03><fC03 i1="15" i2="X" l="SPA"><s0>Sinovial</s0><s5>21</s5></fC03><fC03 i1="16" i2="X" l="FRE"><s0>Chronique</s0><s5>25</s5></fC03><fC03 i1="16" i2="X" l="ENG"><s0>Chronic</s0><s5>25</s5></fC03><fC03 i1="16" i2="X" l="SPA"><s0>Crónico</s0><s5>25</s5></fC03><fC07 i1="01" i2="X" l="FRE"><s0>Système ostéoarticulaire pathologie</s0><s5>37</s5></fC07><fC07 i1="01" i2="X" l="ENG"><s0>Diseases of the osteoarticular system</s0><s5>37</s5></fC07><fC07 i1="01" i2="X" l="SPA"><s0>Sistema osteoarticular patología</s0><s5>37</s5></fC07><fC07 i1="02" i2="X" l="FRE"><s0>Rhumatisme inflammatoire</s0><s5>38</s5></fC07><fC07 i1="02" i2="X" l="ENG"><s0>Inflammatory joint disease</s0><s5>38</s5></fC07><fC07 i1="02" i2="X" l="SPA"><s0>Reumatismo inflamatorio</s0><s5>38</s5></fC07><fC07 i1="03" i2="X" l="FRE"><s0>Immunopathologie</s0><s5>39</s5></fC07><fC07 i1="03" i2="X" l="ENG"><s0>Immunopathology</s0><s5>39</s5></fC07><fC07 i1="03" i2="X" l="SPA"><s0>Inmunopatología</s0><s5>39</s5></fC07><fC07 i1="04" i2="X" l="FRE"><s0>Maladie autoimmune</s0><s5>40</s5></fC07><fC07 i1="04" i2="X" l="ENG"><s0>Autoimmune disease</s0><s5>40</s5></fC07><fC07 i1="04" i2="X" l="SPA"><s0>Enfermedad autoinmune</s0><s5>40</s5></fC07><fN21><s1>083</s1></fN21></pA></standard></inist><affiliations><list><country><li>Allemagne</li></country></list><tree><country name="Allemagne"><noRegion><name sortKey="Voswinkel, J" sort="Voswinkel, J" uniqKey="Voswinkel J" first="J." last="Voswinkel">J. Voswinkel</name></noRegion><name sortKey="Carbon, G" sort="Carbon, G" uniqKey="Carbon G" first="G." last="Carbon">G. Carbon</name><name sortKey="Gause, A" sort="Gause, A" uniqKey="Gause A" first="A." last="Gause">A. Gause</name><name sortKey="Hopf, T" sort="Hopf, T" uniqKey="Hopf T" first="T." last="Hopf">T. Hopf</name><name sortKey="Pfreundschuh, M" sort="Pfreundschuh, M" uniqKey="Pfreundschuh M" first="M." last="Pfreundschuh">M. Pfreundschuh</name><name sortKey="Trumper, L" sort="Trumper, L" uniqKey="Trumper L" first="L." last="Trümper">L. Trümper</name></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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