Experimental allergic encephalomyelitis: the balance between encephalitogenic T lymphocytes and demyelinating antibodies determines size and structure of demyelinated lesions
Summary The effect of a circulating monoclonal antibody recognizing an antigen located on the surface of myelin sheaths (myelin/oligodendroglia glycoprotein, MOG) on clinical and histopathological expression of experimental allergic encephalomyelitis (EAE) was tested in a model of EAE passively tran...
Ausführliche Beschreibung
Gespeichert in:
| Autor*in: |
|---|
| Format: |
E-Artikel |
|---|---|
| Sprache: |
Englisch |
| Erschienen: |
1988 |
|---|
| Umfang: |
11 |
|---|
| Reproduktion: |
Springer Online Journal Archives 1860-2002 |
|---|---|
| Übergeordnetes Werk: |
in: Acta neuropathologica - 1961, 75(1988) vom: Juni, Seite 566-576 |
| Übergeordnetes Werk: |
volume:75 ; year:1988 ; month:06 ; pages:566-576 ; extent:11 |
| Links: |
|---|
| Katalog-ID: |
NLEJ203598784 |
|---|
| LEADER | 01000caa a22002652 4500 | ||
|---|---|---|---|
| 001 | NLEJ203598784 | ||
| 003 | DE-627 | ||
| 005 | 20230506075532.0 | ||
| 007 | cr uuu---uuuuu | ||
| 008 | 070528s1988 xx |||||o 00| ||eng c | ||
| 035 | |a (DE-627)NLEJ203598784 | ||
| 040 | |a DE-627 |b ger |c DE-627 |e rakwb | ||
| 041 | |a eng | ||
| 245 | 1 | 0 | |a Experimental allergic encephalomyelitis: the balance between encephalitogenic T lymphocytes and demyelinating antibodies determines size and structure of demyelinated lesions |
| 264 | 1 | |c 1988 | |
| 300 | |a 11 | ||
| 336 | |a nicht spezifiziert |b zzz |2 rdacontent | ||
| 337 | |a nicht spezifiziert |b z |2 rdamedia | ||
| 338 | |a nicht spezifiziert |b zu |2 rdacarrier | ||
| 520 | |a Summary The effect of a circulating monoclonal antibody recognizing an antigen located on the surface of myelin sheaths (myelin/oligodendroglia glycoprotein, MOG) on clinical and histopathological expression of experimental allergic encephalomyelitis (EAE) was tested in a model of EAE passively transferred by monospecific T lymphocytes. Intravenous injection of anti-MOG antibody at the onset of the disease massively augmented clinical impairment as well as primary demyelination. The structure of the CNS lesions depended on the balance between encephalitogenic T cells and anti-MOG antibody: when EAE was induced with high numbers of T cells, circulating anti-MOG antibody resulted in ubiquitous perivenous demyelination in the spinal cord and medulla oblongata. On the contrary, focal confluent demyelinated lesions were observed in animals injected with low numbers of T cells (even as few as 104) and anti-MOG antibody. Our studies, thus, indicate that the formation of inflammatory demyelinating lesions may be due to a synergistic action of cellular and humoral immune mechanisms. | ||
| 533 | |f Springer Online Journal Archives 1860-2002 | ||
| 700 | 1 | |a Lassmann, H. |4 oth | |
| 700 | 1 | |a Brunner, C. |4 oth | |
| 700 | 1 | |a Bradl, M. |4 oth | |
| 700 | 1 | |a Linington, C. |4 oth | |
| 773 | 0 | 8 | |i in |t Acta neuropathologica |d 1961 |g 75(1988) vom: Juni, Seite 566-576 |w (DE-627)NLEJ188990917 |w (DE-600)1458410-4 |x 1432-0533 |7 nnns |
| 773 | 1 | 8 | |g volume:75 |g year:1988 |g month:06 |g pages:566-576 |g extent:11 |
| 856 | 4 | 0 | |u http://dx.doi.org/10.1007/BF00686201 |
| 912 | |a GBV_USEFLAG_U | ||
| 912 | |a ZDB-1-SOJ | ||
| 912 | |a GBV_NL_ARTICLE | ||
| 951 | |a AR | ||
| 952 | |d 75 |j 1988 |c 6 |h 566-576 |g 11 | ||
| matchkey_str |
article:14320533:1988----::xeietllegcnehlmeiiteaacbtennehltgnclmhctsndmeiaignioiseem |
|---|---|
| hierarchy_sort_str |
1988 |
| publishDate |
1988 |
| allfields |
(DE-627)NLEJ203598784 DE-627 ger DE-627 rakwb eng Experimental allergic encephalomyelitis: the balance between encephalitogenic T lymphocytes and demyelinating antibodies determines size and structure of demyelinated lesions 1988 11 nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier Summary The effect of a circulating monoclonal antibody recognizing an antigen located on the surface of myelin sheaths (myelin/oligodendroglia glycoprotein, MOG) on clinical and histopathological expression of experimental allergic encephalomyelitis (EAE) was tested in a model of EAE passively transferred by monospecific T lymphocytes. Intravenous injection of anti-MOG antibody at the onset of the disease massively augmented clinical impairment as well as primary demyelination. The structure of the CNS lesions depended on the balance between encephalitogenic T cells and anti-MOG antibody: when EAE was induced with high numbers of T cells, circulating anti-MOG antibody resulted in ubiquitous perivenous demyelination in the spinal cord and medulla oblongata. On the contrary, focal confluent demyelinated lesions were observed in animals injected with low numbers of T cells (even as few as 104) and anti-MOG antibody. Our studies, thus, indicate that the formation of inflammatory demyelinating lesions may be due to a synergistic action of cellular and humoral immune mechanisms. Springer Online Journal Archives 1860-2002 Lassmann, H. oth Brunner, C. oth Bradl, M. oth Linington, C. oth in Acta neuropathologica 1961 75(1988) vom: Juni, Seite 566-576 (DE-627)NLEJ188990917 (DE-600)1458410-4 1432-0533 nnns volume:75 year:1988 month:06 pages:566-576 extent:11 http://dx.doi.org/10.1007/BF00686201 GBV_USEFLAG_U ZDB-1-SOJ GBV_NL_ARTICLE AR 75 1988 6 566-576 11 |
| spelling |
(DE-627)NLEJ203598784 DE-627 ger DE-627 rakwb eng Experimental allergic encephalomyelitis: the balance between encephalitogenic T lymphocytes and demyelinating antibodies determines size and structure of demyelinated lesions 1988 11 nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier Summary The effect of a circulating monoclonal antibody recognizing an antigen located on the surface of myelin sheaths (myelin/oligodendroglia glycoprotein, MOG) on clinical and histopathological expression of experimental allergic encephalomyelitis (EAE) was tested in a model of EAE passively transferred by monospecific T lymphocytes. Intravenous injection of anti-MOG antibody at the onset of the disease massively augmented clinical impairment as well as primary demyelination. The structure of the CNS lesions depended on the balance between encephalitogenic T cells and anti-MOG antibody: when EAE was induced with high numbers of T cells, circulating anti-MOG antibody resulted in ubiquitous perivenous demyelination in the spinal cord and medulla oblongata. On the contrary, focal confluent demyelinated lesions were observed in animals injected with low numbers of T cells (even as few as 104) and anti-MOG antibody. Our studies, thus, indicate that the formation of inflammatory demyelinating lesions may be due to a synergistic action of cellular and humoral immune mechanisms. Springer Online Journal Archives 1860-2002 Lassmann, H. oth Brunner, C. oth Bradl, M. oth Linington, C. oth in Acta neuropathologica 1961 75(1988) vom: Juni, Seite 566-576 (DE-627)NLEJ188990917 (DE-600)1458410-4 1432-0533 nnns volume:75 year:1988 month:06 pages:566-576 extent:11 http://dx.doi.org/10.1007/BF00686201 GBV_USEFLAG_U ZDB-1-SOJ GBV_NL_ARTICLE AR 75 1988 6 566-576 11 |
| allfields_unstemmed |
(DE-627)NLEJ203598784 DE-627 ger DE-627 rakwb eng Experimental allergic encephalomyelitis: the balance between encephalitogenic T lymphocytes and demyelinating antibodies determines size and structure of demyelinated lesions 1988 11 nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier Summary The effect of a circulating monoclonal antibody recognizing an antigen located on the surface of myelin sheaths (myelin/oligodendroglia glycoprotein, MOG) on clinical and histopathological expression of experimental allergic encephalomyelitis (EAE) was tested in a model of EAE passively transferred by monospecific T lymphocytes. Intravenous injection of anti-MOG antibody at the onset of the disease massively augmented clinical impairment as well as primary demyelination. The structure of the CNS lesions depended on the balance between encephalitogenic T cells and anti-MOG antibody: when EAE was induced with high numbers of T cells, circulating anti-MOG antibody resulted in ubiquitous perivenous demyelination in the spinal cord and medulla oblongata. On the contrary, focal confluent demyelinated lesions were observed in animals injected with low numbers of T cells (even as few as 104) and anti-MOG antibody. Our studies, thus, indicate that the formation of inflammatory demyelinating lesions may be due to a synergistic action of cellular and humoral immune mechanisms. Springer Online Journal Archives 1860-2002 Lassmann, H. oth Brunner, C. oth Bradl, M. oth Linington, C. oth in Acta neuropathologica 1961 75(1988) vom: Juni, Seite 566-576 (DE-627)NLEJ188990917 (DE-600)1458410-4 1432-0533 nnns volume:75 year:1988 month:06 pages:566-576 extent:11 http://dx.doi.org/10.1007/BF00686201 GBV_USEFLAG_U ZDB-1-SOJ GBV_NL_ARTICLE AR 75 1988 6 566-576 11 |
| allfieldsGer |
(DE-627)NLEJ203598784 DE-627 ger DE-627 rakwb eng Experimental allergic encephalomyelitis: the balance between encephalitogenic T lymphocytes and demyelinating antibodies determines size and structure of demyelinated lesions 1988 11 nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier Summary The effect of a circulating monoclonal antibody recognizing an antigen located on the surface of myelin sheaths (myelin/oligodendroglia glycoprotein, MOG) on clinical and histopathological expression of experimental allergic encephalomyelitis (EAE) was tested in a model of EAE passively transferred by monospecific T lymphocytes. Intravenous injection of anti-MOG antibody at the onset of the disease massively augmented clinical impairment as well as primary demyelination. The structure of the CNS lesions depended on the balance between encephalitogenic T cells and anti-MOG antibody: when EAE was induced with high numbers of T cells, circulating anti-MOG antibody resulted in ubiquitous perivenous demyelination in the spinal cord and medulla oblongata. On the contrary, focal confluent demyelinated lesions were observed in animals injected with low numbers of T cells (even as few as 104) and anti-MOG antibody. Our studies, thus, indicate that the formation of inflammatory demyelinating lesions may be due to a synergistic action of cellular and humoral immune mechanisms. Springer Online Journal Archives 1860-2002 Lassmann, H. oth Brunner, C. oth Bradl, M. oth Linington, C. oth in Acta neuropathologica 1961 75(1988) vom: Juni, Seite 566-576 (DE-627)NLEJ188990917 (DE-600)1458410-4 1432-0533 nnns volume:75 year:1988 month:06 pages:566-576 extent:11 http://dx.doi.org/10.1007/BF00686201 GBV_USEFLAG_U ZDB-1-SOJ GBV_NL_ARTICLE AR 75 1988 6 566-576 11 |
| allfieldsSound |
(DE-627)NLEJ203598784 DE-627 ger DE-627 rakwb eng Experimental allergic encephalomyelitis: the balance between encephalitogenic T lymphocytes and demyelinating antibodies determines size and structure of demyelinated lesions 1988 11 nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier Summary The effect of a circulating monoclonal antibody recognizing an antigen located on the surface of myelin sheaths (myelin/oligodendroglia glycoprotein, MOG) on clinical and histopathological expression of experimental allergic encephalomyelitis (EAE) was tested in a model of EAE passively transferred by monospecific T lymphocytes. Intravenous injection of anti-MOG antibody at the onset of the disease massively augmented clinical impairment as well as primary demyelination. The structure of the CNS lesions depended on the balance between encephalitogenic T cells and anti-MOG antibody: when EAE was induced with high numbers of T cells, circulating anti-MOG antibody resulted in ubiquitous perivenous demyelination in the spinal cord and medulla oblongata. On the contrary, focal confluent demyelinated lesions were observed in animals injected with low numbers of T cells (even as few as 104) and anti-MOG antibody. Our studies, thus, indicate that the formation of inflammatory demyelinating lesions may be due to a synergistic action of cellular and humoral immune mechanisms. Springer Online Journal Archives 1860-2002 Lassmann, H. oth Brunner, C. oth Bradl, M. oth Linington, C. oth in Acta neuropathologica 1961 75(1988) vom: Juni, Seite 566-576 (DE-627)NLEJ188990917 (DE-600)1458410-4 1432-0533 nnns volume:75 year:1988 month:06 pages:566-576 extent:11 http://dx.doi.org/10.1007/BF00686201 GBV_USEFLAG_U ZDB-1-SOJ GBV_NL_ARTICLE AR 75 1988 6 566-576 11 |
| language |
English |
| source |
in Acta neuropathologica 75(1988) vom: Juni, Seite 566-576 volume:75 year:1988 month:06 pages:566-576 extent:11 |
| sourceStr |
in Acta neuropathologica 75(1988) vom: Juni, Seite 566-576 volume:75 year:1988 month:06 pages:566-576 extent:11 |
| format_phy_str_mv |
Article |
| institution |
findex.gbv.de |
| isfreeaccess_bool |
false |
| container_title |
Acta neuropathologica |
| authorswithroles_txt_mv |
Lassmann, H. @@oth@@ Brunner, C. @@oth@@ Bradl, M. @@oth@@ Linington, C. @@oth@@ |
| publishDateDaySort_date |
1988-06-01T00:00:00Z |
| hierarchy_top_id |
NLEJ188990917 |
| id |
NLEJ203598784 |
| language_de |
englisch |
| fullrecord |
<?xml version="1.0" encoding="UTF-8"?><collection xmlns="http://www.loc.gov/MARC21/slim"><record><leader>01000caa a22002652 4500</leader><controlfield tag="001">NLEJ203598784</controlfield><controlfield tag="003">DE-627</controlfield><controlfield tag="005">20230506075532.0</controlfield><controlfield tag="007">cr uuu---uuuuu</controlfield><controlfield tag="008">070528s1988 xx |||||o 00| ||eng c</controlfield><datafield tag="035" ind1=" " ind2=" "><subfield code="a">(DE-627)NLEJ203598784</subfield></datafield><datafield tag="040" ind1=" " ind2=" "><subfield code="a">DE-627</subfield><subfield code="b">ger</subfield><subfield code="c">DE-627</subfield><subfield code="e">rakwb</subfield></datafield><datafield tag="041" ind1=" " ind2=" "><subfield code="a">eng</subfield></datafield><datafield tag="245" ind1="1" ind2="0"><subfield code="a">Experimental allergic encephalomyelitis: the balance between encephalitogenic T lymphocytes and demyelinating antibodies determines size and structure of demyelinated lesions</subfield></datafield><datafield tag="264" ind1=" " ind2="1"><subfield code="c">1988</subfield></datafield><datafield tag="300" ind1=" " ind2=" "><subfield code="a">11</subfield></datafield><datafield tag="336" ind1=" " ind2=" "><subfield code="a">nicht spezifiziert</subfield><subfield code="b">zzz</subfield><subfield code="2">rdacontent</subfield></datafield><datafield tag="337" ind1=" " ind2=" "><subfield code="a">nicht spezifiziert</subfield><subfield code="b">z</subfield><subfield code="2">rdamedia</subfield></datafield><datafield tag="338" ind1=" " ind2=" "><subfield code="a">nicht spezifiziert</subfield><subfield code="b">zu</subfield><subfield code="2">rdacarrier</subfield></datafield><datafield tag="520" ind1=" " ind2=" "><subfield code="a">Summary The effect of a circulating monoclonal antibody recognizing an antigen located on the surface of myelin sheaths (myelin/oligodendroglia glycoprotein, MOG) on clinical and histopathological expression of experimental allergic encephalomyelitis (EAE) was tested in a model of EAE passively transferred by monospecific T lymphocytes. Intravenous injection of anti-MOG antibody at the onset of the disease massively augmented clinical impairment as well as primary demyelination. The structure of the CNS lesions depended on the balance between encephalitogenic T cells and anti-MOG antibody: when EAE was induced with high numbers of T cells, circulating anti-MOG antibody resulted in ubiquitous perivenous demyelination in the spinal cord and medulla oblongata. On the contrary, focal confluent demyelinated lesions were observed in animals injected with low numbers of T cells (even as few as 104) and anti-MOG antibody. Our studies, thus, indicate that the formation of inflammatory demyelinating lesions may be due to a synergistic action of cellular and humoral immune mechanisms.</subfield></datafield><datafield tag="533" ind1=" " ind2=" "><subfield code="f">Springer Online Journal Archives 1860-2002</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Lassmann, H.</subfield><subfield code="4">oth</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Brunner, C.</subfield><subfield code="4">oth</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Bradl, M.</subfield><subfield code="4">oth</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Linington, C.</subfield><subfield code="4">oth</subfield></datafield><datafield tag="773" ind1="0" ind2="8"><subfield code="i">in</subfield><subfield code="t">Acta neuropathologica</subfield><subfield code="d">1961</subfield><subfield code="g">75(1988) vom: Juni, Seite 566-576</subfield><subfield code="w">(DE-627)NLEJ188990917</subfield><subfield code="w">(DE-600)1458410-4</subfield><subfield code="x">1432-0533</subfield><subfield code="7">nnns</subfield></datafield><datafield tag="773" ind1="1" ind2="8"><subfield code="g">volume:75</subfield><subfield code="g">year:1988</subfield><subfield code="g">month:06</subfield><subfield code="g">pages:566-576</subfield><subfield code="g">extent:11</subfield></datafield><datafield tag="856" ind1="4" ind2="0"><subfield code="u">http://dx.doi.org/10.1007/BF00686201</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_USEFLAG_U</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">ZDB-1-SOJ</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_NL_ARTICLE</subfield></datafield><datafield tag="951" ind1=" " ind2=" "><subfield code="a">AR</subfield></datafield><datafield tag="952" ind1=" " ind2=" "><subfield code="d">75</subfield><subfield code="j">1988</subfield><subfield code="c">6</subfield><subfield code="h">566-576</subfield><subfield code="g">11</subfield></datafield></record></collection>
|
| series2 |
Springer Online Journal Archives 1860-2002 |
| ppnlink_with_tag_str_mv |
@@773@@(DE-627)NLEJ188990917 |
| format |
electronic Article |
| delete_txt_mv |
keep |
| collection |
NL |
| remote_str |
true |
| illustrated |
Not Illustrated |
| issn |
1432-0533 |
| topic_title |
Experimental allergic encephalomyelitis: the balance between encephalitogenic T lymphocytes and demyelinating antibodies determines size and structure of demyelinated lesions |
| format_facet |
Elektronische Aufsätze Aufsätze Elektronische Ressource |
| format_main_str_mv |
Text Zeitschrift/Artikel |
| carriertype_str_mv |
zu |
| author2_variant |
h l hl c b cb m b mb c l cl |
| hierarchy_parent_title |
Acta neuropathologica |
| hierarchy_parent_id |
NLEJ188990917 |
| hierarchy_top_title |
Acta neuropathologica |
| isfreeaccess_txt |
false |
| familylinks_str_mv |
(DE-627)NLEJ188990917 (DE-600)1458410-4 |
| title |
Experimental allergic encephalomyelitis: the balance between encephalitogenic T lymphocytes and demyelinating antibodies determines size and structure of demyelinated lesions |
| spellingShingle |
Experimental allergic encephalomyelitis: the balance between encephalitogenic T lymphocytes and demyelinating antibodies determines size and structure of demyelinated lesions |
| ctrlnum |
(DE-627)NLEJ203598784 |
| title_full |
Experimental allergic encephalomyelitis: the balance between encephalitogenic T lymphocytes and demyelinating antibodies determines size and structure of demyelinated lesions |
| journal |
Acta neuropathologica |
| journalStr |
Acta neuropathologica |
| lang_code |
eng |
| isOA_bool |
false |
| recordtype |
marc |
| publishDateSort |
1988 |
| contenttype_str_mv |
zzz |
| container_start_page |
566 |
| container_volume |
75 |
| physical |
11 |
| format_se |
Elektronische Aufsätze |
| title_sort |
experimental allergic encephalomyelitis: the balance between encephalitogenic t lymphocytes and demyelinating antibodies determines size and structure of demyelinated lesions |
| title_auth |
Experimental allergic encephalomyelitis: the balance between encephalitogenic T lymphocytes and demyelinating antibodies determines size and structure of demyelinated lesions |
| abstract |
Summary The effect of a circulating monoclonal antibody recognizing an antigen located on the surface of myelin sheaths (myelin/oligodendroglia glycoprotein, MOG) on clinical and histopathological expression of experimental allergic encephalomyelitis (EAE) was tested in a model of EAE passively transferred by monospecific T lymphocytes. Intravenous injection of anti-MOG antibody at the onset of the disease massively augmented clinical impairment as well as primary demyelination. The structure of the CNS lesions depended on the balance between encephalitogenic T cells and anti-MOG antibody: when EAE was induced with high numbers of T cells, circulating anti-MOG antibody resulted in ubiquitous perivenous demyelination in the spinal cord and medulla oblongata. On the contrary, focal confluent demyelinated lesions were observed in animals injected with low numbers of T cells (even as few as 104) and anti-MOG antibody. Our studies, thus, indicate that the formation of inflammatory demyelinating lesions may be due to a synergistic action of cellular and humoral immune mechanisms. |
| abstractGer |
Summary The effect of a circulating monoclonal antibody recognizing an antigen located on the surface of myelin sheaths (myelin/oligodendroglia glycoprotein, MOG) on clinical and histopathological expression of experimental allergic encephalomyelitis (EAE) was tested in a model of EAE passively transferred by monospecific T lymphocytes. Intravenous injection of anti-MOG antibody at the onset of the disease massively augmented clinical impairment as well as primary demyelination. The structure of the CNS lesions depended on the balance between encephalitogenic T cells and anti-MOG antibody: when EAE was induced with high numbers of T cells, circulating anti-MOG antibody resulted in ubiquitous perivenous demyelination in the spinal cord and medulla oblongata. On the contrary, focal confluent demyelinated lesions were observed in animals injected with low numbers of T cells (even as few as 104) and anti-MOG antibody. Our studies, thus, indicate that the formation of inflammatory demyelinating lesions may be due to a synergistic action of cellular and humoral immune mechanisms. |
| abstract_unstemmed |
Summary The effect of a circulating monoclonal antibody recognizing an antigen located on the surface of myelin sheaths (myelin/oligodendroglia glycoprotein, MOG) on clinical and histopathological expression of experimental allergic encephalomyelitis (EAE) was tested in a model of EAE passively transferred by monospecific T lymphocytes. Intravenous injection of anti-MOG antibody at the onset of the disease massively augmented clinical impairment as well as primary demyelination. The structure of the CNS lesions depended on the balance between encephalitogenic T cells and anti-MOG antibody: when EAE was induced with high numbers of T cells, circulating anti-MOG antibody resulted in ubiquitous perivenous demyelination in the spinal cord and medulla oblongata. On the contrary, focal confluent demyelinated lesions were observed in animals injected with low numbers of T cells (even as few as 104) and anti-MOG antibody. Our studies, thus, indicate that the formation of inflammatory demyelinating lesions may be due to a synergistic action of cellular and humoral immune mechanisms. |
| collection_details |
GBV_USEFLAG_U ZDB-1-SOJ GBV_NL_ARTICLE |
| title_short |
Experimental allergic encephalomyelitis: the balance between encephalitogenic T lymphocytes and demyelinating antibodies determines size and structure of demyelinated lesions |
| url |
http://dx.doi.org/10.1007/BF00686201 |
| remote_bool |
true |
| author2 |
Lassmann, H. Brunner, C. Bradl, M. Linington, C. |
| author2Str |
Lassmann, H. Brunner, C. Bradl, M. Linington, C. |
| ppnlink |
NLEJ188990917 |
| mediatype_str_mv |
z |
| isOA_txt |
false |
| hochschulschrift_bool |
false |
| author2_role |
oth oth oth oth |
| up_date |
2024-07-05T21:53:14.632Z |
| _version_ |
1803777626217644032 |
| fullrecord_marcxml |
<?xml version="1.0" encoding="UTF-8"?><collection xmlns="http://www.loc.gov/MARC21/slim"><record><leader>01000caa a22002652 4500</leader><controlfield tag="001">NLEJ203598784</controlfield><controlfield tag="003">DE-627</controlfield><controlfield tag="005">20230506075532.0</controlfield><controlfield tag="007">cr uuu---uuuuu</controlfield><controlfield tag="008">070528s1988 xx |||||o 00| ||eng c</controlfield><datafield tag="035" ind1=" " ind2=" "><subfield code="a">(DE-627)NLEJ203598784</subfield></datafield><datafield tag="040" ind1=" " ind2=" "><subfield code="a">DE-627</subfield><subfield code="b">ger</subfield><subfield code="c">DE-627</subfield><subfield code="e">rakwb</subfield></datafield><datafield tag="041" ind1=" " ind2=" "><subfield code="a">eng</subfield></datafield><datafield tag="245" ind1="1" ind2="0"><subfield code="a">Experimental allergic encephalomyelitis: the balance between encephalitogenic T lymphocytes and demyelinating antibodies determines size and structure of demyelinated lesions</subfield></datafield><datafield tag="264" ind1=" " ind2="1"><subfield code="c">1988</subfield></datafield><datafield tag="300" ind1=" " ind2=" "><subfield code="a">11</subfield></datafield><datafield tag="336" ind1=" " ind2=" "><subfield code="a">nicht spezifiziert</subfield><subfield code="b">zzz</subfield><subfield code="2">rdacontent</subfield></datafield><datafield tag="337" ind1=" " ind2=" "><subfield code="a">nicht spezifiziert</subfield><subfield code="b">z</subfield><subfield code="2">rdamedia</subfield></datafield><datafield tag="338" ind1=" " ind2=" "><subfield code="a">nicht spezifiziert</subfield><subfield code="b">zu</subfield><subfield code="2">rdacarrier</subfield></datafield><datafield tag="520" ind1=" " ind2=" "><subfield code="a">Summary The effect of a circulating monoclonal antibody recognizing an antigen located on the surface of myelin sheaths (myelin/oligodendroglia glycoprotein, MOG) on clinical and histopathological expression of experimental allergic encephalomyelitis (EAE) was tested in a model of EAE passively transferred by monospecific T lymphocytes. Intravenous injection of anti-MOG antibody at the onset of the disease massively augmented clinical impairment as well as primary demyelination. The structure of the CNS lesions depended on the balance between encephalitogenic T cells and anti-MOG antibody: when EAE was induced with high numbers of T cells, circulating anti-MOG antibody resulted in ubiquitous perivenous demyelination in the spinal cord and medulla oblongata. On the contrary, focal confluent demyelinated lesions were observed in animals injected with low numbers of T cells (even as few as 104) and anti-MOG antibody. Our studies, thus, indicate that the formation of inflammatory demyelinating lesions may be due to a synergistic action of cellular and humoral immune mechanisms.</subfield></datafield><datafield tag="533" ind1=" " ind2=" "><subfield code="f">Springer Online Journal Archives 1860-2002</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Lassmann, H.</subfield><subfield code="4">oth</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Brunner, C.</subfield><subfield code="4">oth</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Bradl, M.</subfield><subfield code="4">oth</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Linington, C.</subfield><subfield code="4">oth</subfield></datafield><datafield tag="773" ind1="0" ind2="8"><subfield code="i">in</subfield><subfield code="t">Acta neuropathologica</subfield><subfield code="d">1961</subfield><subfield code="g">75(1988) vom: Juni, Seite 566-576</subfield><subfield code="w">(DE-627)NLEJ188990917</subfield><subfield code="w">(DE-600)1458410-4</subfield><subfield code="x">1432-0533</subfield><subfield code="7">nnns</subfield></datafield><datafield tag="773" ind1="1" ind2="8"><subfield code="g">volume:75</subfield><subfield code="g">year:1988</subfield><subfield code="g">month:06</subfield><subfield code="g">pages:566-576</subfield><subfield code="g">extent:11</subfield></datafield><datafield tag="856" ind1="4" ind2="0"><subfield code="u">http://dx.doi.org/10.1007/BF00686201</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_USEFLAG_U</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">ZDB-1-SOJ</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_NL_ARTICLE</subfield></datafield><datafield tag="951" ind1=" " ind2=" "><subfield code="a">AR</subfield></datafield><datafield tag="952" ind1=" " ind2=" "><subfield code="d">75</subfield><subfield code="j">1988</subfield><subfield code="c">6</subfield><subfield code="h">566-576</subfield><subfield code="g">11</subfield></datafield></record></collection>
|
| score |
7.398958 |