Colocalization of C4d deposits/CD68+ macrophages in rheumatoid nodule and granuloma annulare: immunohistochemical evidence of a complement-mediated mechanism in fibrinoid necrosis.
Identifieur interne : 000635 ( PubMed/Corpus ); précédent : 000634; suivant : 000636Colocalization of C4d deposits/CD68+ macrophages in rheumatoid nodule and granuloma annulare: immunohistochemical evidence of a complement-mediated mechanism in fibrinoid necrosis.
Auteurs : M. Knoess ; M G Krukemeyer ; J. Kriegsmann ; H. Thabe ; M. Otto ; V. KrennSource :
- Pathology, research and practice [ 0344-0338 ] ; 2008.
English descriptors
- KwdEn :
- Adolescent, Adult, Aged, Aged, 80 and over, Antigens, CD (metabolism), Antigens, Differentiation, Myelomonocytic (metabolism), Biomarkers (metabolism), Child, Child, Preschool, Complement C4b (metabolism), Female, Granuloma Annulare (metabolism), Granuloma Annulare (pathology), Humans, Immunoenzyme Techniques, Macrophages (metabolism), Macrophages (pathology), Male, Middle Aged, Necrosis, Peptide Fragments (metabolism), Rheumatoid Nodule (metabolism), Rheumatoid Nodule (pathology).
- MESH :
- chemical , metabolism : Antigens, CD, Antigens, Differentiation, Myelomonocytic, Biomarkers, Complement C4b, Peptide Fragments.
- metabolism : Granuloma Annulare, Macrophages, Rheumatoid Nodule.
- pathology : Granuloma Annulare, Macrophages, Rheumatoid Nodule.
- Adolescent, Adult, Aged, Aged, 80 and over, Child, Child, Preschool, Female, Humans, Immunoenzyme Techniques, Male, Middle Aged, Necrosis.
Abstract
Rheumatoid nodule (RN) represents a palisading granuloma with central fibrinoid necrosis, which is not only a classical manifestation of rheumatoid arthritis (RA) and part of the American College of Rheumatology (ACR)-criteria, but also is its diagnostic hallmark. The pathogenesis of RN is still not fully understood. At present, only data on serum analyses indicating a complement-mediated pathogenesis in the development of RA are available. Equivalent examinations for RN have not yet been performed. Granuloma annulare (GA) represents another type of palisading granuloma. A special subtype of GA, subcutaneous GA (SGA), is an important differential diagnosis to RN. Therefore, our aim was to examine RN and SGA regarding the complement deposition (C4d) by immunohistochemical means. All RN and GA were stained by hematoxylin/eosin and different special stains. In addition, all specimens were stained immunohistochemically with antibodies against CD68. Five GA and five RN were analyzed immunohistochemically with antibodies against C4d and CD68, and evaluated using single- and doublestaining immunohistochemistry. All RN and GA displayed depositions of C4d within their central necroses and between the surrounding palisading macrophages. Most importantly, C4d/CD68 double staining was visible in the palisading macrophages next to the necroses, while macrophages in the periphery were negative for C4d but positive for CD68. The main difference between RN and GA was a quantitative phenomenon with less positively reacting macrophages in a more incomplete palisade in GA. The positive reactions of all central necroses to C4d and colocalization of CD68 and C4d suggest that a complement-mediated mechanism may be operative in the formation of fibrinoid necrosis. This mechanism may be involved in any form of "fibrinoid necrosis", since no different patterns of C4d/CD68 expression could be observed in GA. This may explain why RG/GA are not distinguishable morphologically.
DOI: 10.1016/j.prp.2008.01.009
PubMed: 18339486
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pubmed:18339486Le document en format XML
<record><TEI><teiHeader><fileDesc><titleStmt><title xml:lang="en">Colocalization of C4d deposits/CD68+ macrophages in rheumatoid nodule and granuloma annulare: immunohistochemical evidence of a complement-mediated mechanism in fibrinoid necrosis.</title><author><name sortKey="Knoess, M" sort="Knoess, M" uniqKey="Knoess M" first="M" last="Knoess">M. Knoess</name><affiliation><nlm:affiliation>Department of Pathology, Institute of Pathology, Max-Planck-Strasse 18+20, Trier, Germany. drknoess@aol.com</nlm:affiliation></affiliation></author><author><name sortKey="Krukemeyer, M G" sort="Krukemeyer, M G" uniqKey="Krukemeyer M" first="M G" last="Krukemeyer">M G Krukemeyer</name></author><author><name sortKey="Kriegsmann, J" sort="Kriegsmann, J" uniqKey="Kriegsmann J" first="J" last="Kriegsmann">J. Kriegsmann</name></author><author><name sortKey="Thabe, H" sort="Thabe, H" uniqKey="Thabe H" first="H" last="Thabe">H. Thabe</name></author><author><name sortKey="Otto, M" sort="Otto, M" uniqKey="Otto M" first="M" last="Otto">M. Otto</name></author><author><name sortKey="Krenn, V" sort="Krenn, V" uniqKey="Krenn V" first="V" last="Krenn">V. Krenn</name></author></titleStmt><publicationStmt><idno type="wicri:source">PubMed</idno><date when="2008">2008</date><idno type="RBID">pubmed:18339486</idno><idno type="pmid">18339486</idno><idno type="doi">10.1016/j.prp.2008.01.009</idno><idno type="wicri:Area/PubMed/Corpus">000635</idno><idno type="wicri:explorRef" wicri:stream="PubMed" wicri:step="Corpus" wicri:corpus="PubMed">000635</idno></publicationStmt><sourceDesc><biblStruct><analytic><title xml:lang="en">Colocalization of C4d deposits/CD68+ macrophages in rheumatoid nodule and granuloma annulare: immunohistochemical evidence of a complement-mediated mechanism in fibrinoid necrosis.</title><author><name sortKey="Knoess, M" sort="Knoess, M" uniqKey="Knoess M" first="M" last="Knoess">M. Knoess</name><affiliation><nlm:affiliation>Department of Pathology, Institute of Pathology, Max-Planck-Strasse 18+20, Trier, Germany. drknoess@aol.com</nlm:affiliation></affiliation></author><author><name sortKey="Krukemeyer, M G" sort="Krukemeyer, M G" uniqKey="Krukemeyer M" first="M G" last="Krukemeyer">M G Krukemeyer</name></author><author><name sortKey="Kriegsmann, J" sort="Kriegsmann, J" uniqKey="Kriegsmann J" first="J" last="Kriegsmann">J. Kriegsmann</name></author><author><name sortKey="Thabe, H" sort="Thabe, H" uniqKey="Thabe H" first="H" last="Thabe">H. Thabe</name></author><author><name sortKey="Otto, M" sort="Otto, M" uniqKey="Otto M" first="M" last="Otto">M. Otto</name></author><author><name sortKey="Krenn, V" sort="Krenn, V" uniqKey="Krenn V" first="V" last="Krenn">V. Krenn</name></author></analytic><series><title level="j">Pathology, research and practice</title><idno type="ISSN">0344-0338</idno><imprint><date when="2008" type="published">2008</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Adolescent</term><term>Adult</term><term>Aged</term><term>Aged, 80 and over</term><term>Antigens, CD (metabolism)</term><term>Antigens, Differentiation, Myelomonocytic (metabolism)</term><term>Biomarkers (metabolism)</term><term>Child</term><term>Child, Preschool</term><term>Complement C4b (metabolism)</term><term>Female</term><term>Granuloma Annulare (metabolism)</term><term>Granuloma Annulare (pathology)</term><term>Humans</term><term>Immunoenzyme Techniques</term><term>Macrophages (metabolism)</term><term>Macrophages (pathology)</term><term>Male</term><term>Middle Aged</term><term>Necrosis</term><term>Peptide Fragments (metabolism)</term><term>Rheumatoid Nodule (metabolism)</term><term>Rheumatoid Nodule (pathology)</term></keywords><keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>Antigens, CD</term><term>Antigens, Differentiation, Myelomonocytic</term><term>Biomarkers</term><term>Complement C4b</term><term>Peptide Fragments</term></keywords><keywords scheme="MESH" qualifier="metabolism" xml:lang="en"><term>Granuloma Annulare</term><term>Macrophages</term><term>Rheumatoid Nodule</term></keywords><keywords scheme="MESH" qualifier="pathology" xml:lang="en"><term>Granuloma Annulare</term><term>Macrophages</term><term>Rheumatoid Nodule</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Adolescent</term><term>Adult</term><term>Aged</term><term>Aged, 80 and over</term><term>Child</term><term>Child, Preschool</term><term>Female</term><term>Humans</term><term>Immunoenzyme Techniques</term><term>Male</term><term>Middle Aged</term><term>Necrosis</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Rheumatoid nodule (RN) represents a palisading granuloma with central fibrinoid necrosis, which is not only a classical manifestation of rheumatoid arthritis (RA) and part of the American College of Rheumatology (ACR)-criteria, but also is its diagnostic hallmark. The pathogenesis of RN is still not fully understood. At present, only data on serum analyses indicating a complement-mediated pathogenesis in the development of RA are available. Equivalent examinations for RN have not yet been performed. Granuloma annulare (GA) represents another type of palisading granuloma. A special subtype of GA, subcutaneous GA (SGA), is an important differential diagnosis to RN. Therefore, our aim was to examine RN and SGA regarding the complement deposition (C4d) by immunohistochemical means. All RN and GA were stained by hematoxylin/eosin and different special stains. In addition, all specimens were stained immunohistochemically with antibodies against CD68. Five GA and five RN were analyzed immunohistochemically with antibodies against C4d and CD68, and evaluated using single- and doublestaining immunohistochemistry. All RN and GA displayed depositions of C4d within their central necroses and between the surrounding palisading macrophages. Most importantly, C4d/CD68 double staining was visible in the palisading macrophages next to the necroses, while macrophages in the periphery were negative for C4d but positive for CD68. The main difference between RN and GA was a quantitative phenomenon with less positively reacting macrophages in a more incomplete palisade in GA. The positive reactions of all central necroses to C4d and colocalization of CD68 and C4d suggest that a complement-mediated mechanism may be operative in the formation of fibrinoid necrosis. This mechanism may be involved in any form of "fibrinoid necrosis", since no different patterns of C4d/CD68 expression could be observed in GA. This may explain why RG/GA are not distinguishable morphologically.</div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">18339486</PMID><DateCreated><Year>2008</Year><Month>05</Month><Day>06</Day></DateCreated><DateCompleted><Year>2008</Year><Month>08</Month><Day>21</Day></DateCompleted><DateRevised><Year>2015</Year><Month>11</Month><Day>19</Day></DateRevised><Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Print">0344-0338</ISSN><JournalIssue CitedMedium="Print"><Volume>204</Volume><Issue>6</Issue><PubDate><Year>2008</Year></PubDate></JournalIssue><Title>Pathology, research and practice</Title><ISOAbbreviation>Pathol. Res. Pract.</ISOAbbreviation></Journal><ArticleTitle>Colocalization of C4d deposits/CD68+ macrophages in rheumatoid nodule and granuloma annulare: immunohistochemical evidence of a complement-mediated mechanism in fibrinoid necrosis.</ArticleTitle><Pagination><MedlinePgn>373-8</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.1016/j.prp.2008.01.009</ELocationID><Abstract><AbstractText>Rheumatoid nodule (RN) represents a palisading granuloma with central fibrinoid necrosis, which is not only a classical manifestation of rheumatoid arthritis (RA) and part of the American College of Rheumatology (ACR)-criteria, but also is its diagnostic hallmark. The pathogenesis of RN is still not fully understood. At present, only data on serum analyses indicating a complement-mediated pathogenesis in the development of RA are available. Equivalent examinations for RN have not yet been performed. Granuloma annulare (GA) represents another type of palisading granuloma. A special subtype of GA, subcutaneous GA (SGA), is an important differential diagnosis to RN. Therefore, our aim was to examine RN and SGA regarding the complement deposition (C4d) by immunohistochemical means. All RN and GA were stained by hematoxylin/eosin and different special stains. In addition, all specimens were stained immunohistochemically with antibodies against CD68. Five GA and five RN were analyzed immunohistochemically with antibodies against C4d and CD68, and evaluated using single- and doublestaining immunohistochemistry. All RN and GA displayed depositions of C4d within their central necroses and between the surrounding palisading macrophages. Most importantly, C4d/CD68 double staining was visible in the palisading macrophages next to the necroses, while macrophages in the periphery were negative for C4d but positive for CD68. The main difference between RN and GA was a quantitative phenomenon with less positively reacting macrophages in a more incomplete palisade in GA. The positive reactions of all central necroses to C4d and colocalization of CD68 and C4d suggest that a complement-mediated mechanism may be operative in the formation of fibrinoid necrosis. This mechanism may be involved in any form of "fibrinoid necrosis", since no different patterns of C4d/CD68 expression could be observed in GA. This may explain why RG/GA are not distinguishable morphologically.</AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Knoess</LastName><ForeName>M</ForeName><Initials>M</Initials><AffiliationInfo><Affiliation>Department of Pathology, Institute of Pathology, Max-Planck-Strasse 18+20, Trier, Germany. drknoess@aol.com</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Krukemeyer</LastName><ForeName>M G</ForeName><Initials>MG</Initials></Author><Author ValidYN="Y"><LastName>Kriegsmann</LastName><ForeName>J</ForeName><Initials>J</Initials></Author><Author ValidYN="Y"><LastName>Thabe</LastName><ForeName>H</ForeName><Initials>H</Initials></Author><Author ValidYN="Y"><LastName>Otto</LastName><ForeName>M</ForeName><Initials>M</Initials></Author><Author ValidYN="Y"><LastName>Krenn</LastName><ForeName>V</ForeName><Initials>V</Initials></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2008</Year><Month>03</Month><Day>14</Day></ArticleDate></Article><MedlineJournalInfo><Country>Germany</Country><MedlineTA>Pathol Res Pract</MedlineTA><NlmUniqueID>7806109</NlmUniqueID><ISSNLinking>0344-0338</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D015703">Antigens, CD</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D015214">Antigens, Differentiation, Myelomonocytic</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D015415">Biomarkers</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="C067980">CD68 antigen, human</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D010446">Peptide Fragments</NameOfSubstance></Chemical><Chemical><RegistryNumber>80295-50-7</RegistryNumber><NameOfSubstance UI="D015935">Complement C4b</NameOfSubstance></Chemical><Chemical><RegistryNumber>80295-52-9</RegistryNumber><NameOfSubstance UI="C032261">complement C4d</NameOfSubstance></Chemical></ChemicalList><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D000293" MajorTopicYN="N">Adolescent</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D000328" MajorTopicYN="N">Adult</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D000368" MajorTopicYN="N">Aged</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D000369" MajorTopicYN="N">Aged, 80 and over</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D015703" MajorTopicYN="N">Antigens, CD</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D015214" MajorTopicYN="N">Antigens, Differentiation, Myelomonocytic</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D015415" MajorTopicYN="N">Biomarkers</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D002648" MajorTopicYN="N">Child</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D002675" MajorTopicYN="N">Child, Preschool</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D015935" MajorTopicYN="N">Complement C4b</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D005260" MajorTopicYN="N">Female</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D016460" MajorTopicYN="N">Granuloma Annulare</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName><QualifierName UI="Q000473" MajorTopicYN="N">pathology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D007124" MajorTopicYN="N">Immunoenzyme Techniques</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D008264" MajorTopicYN="N">Macrophages</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName><QualifierName UI="Q000473" MajorTopicYN="N">pathology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D008297" MajorTopicYN="N">Male</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D008875" MajorTopicYN="N">Middle Aged</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D009336" MajorTopicYN="N">Necrosis</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D010446" MajorTopicYN="N">Peptide Fragments</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D012218" MajorTopicYN="N">Rheumatoid Nodule</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName><QualifierName UI="Q000473" MajorTopicYN="N">pathology</QualifierName></MeshHeading></MeshHeadingList></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="received"><Year>2007</Year><Month>05</Month><Day>10</Day></PubMedPubDate><PubMedPubDate PubStatus="revised"><Year>2007</Year><Month>12</Month><Day>30</Day></PubMedPubDate><PubMedPubDate PubStatus="accepted"><Year>2008</Year><Month>01</Month><Day>11</Day></PubMedPubDate><PubMedPubDate PubStatus="pubmed"><Year>2008</Year><Month>3</Month><Day>15</Day><Hour>9</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2008</Year><Month>8</Month><Day>22</Day><Hour>9</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2008</Year><Month>3</Month><Day>15</Day><Hour>9</Hour><Minute>0</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">18339486</ArticleId><ArticleId IdType="pii">S0344-0338(08)00027-7</ArticleId><ArticleId IdType="doi">10.1016/j.prp.2008.01.009</ArticleId></ArticleIdList></PubmedData></pubmed></record>Pour manipuler ce document sous Unix (Dilib)
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