GLORIA

GEOMAR Library Ocean Research Information Access

X

Your email was sent successfully. Check your inbox.

An error occurred while sending the email. Please try again.

Proceed reservation?

Export
Filter
  • The American Association of Immunologists  (4)
Material
Publisher
  • The American Association of Immunologists  (4)
Person/Organisation
Language
Years
Subjects(RVK)
  • 1
    Online Resource
    Online Resource
    Age-related resistance to experimental autoimmune myasthenia gravis in rats.
    The American Association of Immunologists ; 1993
    In:  The Journal of Immunology Vol. 150, No. 9 ( 1993-05-01), p. 4093-4103
    Details
    In: The Journal of Immunology, The American Association of Immunologists, Vol. 150, No. 9 ( 1993-05-01), p. 4093-4103
    Abstract: The influence of age on the induction of experimental autoimmune myasthenia gravis (EAMG) was investigated. Immunization with acetylcholine receptor (AChR) or injection of varying amounts of anti-AChR mAb 35 into young adult (10-12 wk) BN rats induced severe signs of EAMG including weight loss and decrement of muscle action potential, whereas aged BN rats (120-130 wk) did not show any clinical signs of EAMG. Serum anti-AChr mAb titers were not significantly different in young and aged rats up to 24 h after administration of mAb. No significant AChR loss was demonstrated in aged rats, whereas similarly treated young rats showed extensive AChR loss. In contrast to young rats, no degradation of the postsynaptic membrane could be demonstrated by electron microscopy in aged rats. C component C3 and C5b-9 membrane attack complex could be demonstrated at the neuromuscular junction in both young and aged mAb-treated rats. However, infiltrating macrophages and necrotic muscle fibers were seen only in young rats. These results suggest that the postsynaptic membrane in aged rats is resistant to autoantibody attack. AChR degradation by antigenic modulation may be less efficient in aged rats as a result of altered AChR density and distribution or rigidity of the postsynaptic membrane. Age-related resistance in the EAMG model can provide more information about the factors that determine the severity of myasthenia gravis. Manipulation of AChR density or lipid composition of the postsynaptic membrane may be of therapeutic interest in myasthenia gravis.
    Type of Medium: Online Resource
    ISSN: 0022-1767 , 1550-6606
    URL: Article
    DOI: 10.4049/jimmunol.150.9.4093
    RVK:
    XA 54100
    RVK:
    XA 10000
    Language: English
    Publisher: The American Association of Immunologists
    Publication Date: 1993
    detail.hit.zdb_id: 1475085-5
    Location Call Number Limitation Availability
    BibTip Others were also interested in ...
    Online Resource
  • 2
    Online Resource
    Online Resource
    Human anti-nicotinic acetylcholine receptor recombinant Fab fragments isolated from thymus-derived phage display libraries from myasthenia gravis patients reflect predominant specificities in serum and block the action of pathogenic serum antibodies.
    The American Association of Immunologists ; 1997
    In:  The Journal of Immunology Vol. 158, No. 4 ( 1997-02-15), p. 1919-1929
    Details
    In: The Journal of Immunology, The American Association of Immunologists, Vol. 158, No. 4 ( 1997-02-15), p. 1919-1929
    Abstract: Myasthenia gravis (MG) is a prototype Ab-mediated autoimmune disease in which Abs against nicotinic acetylcholine receptors (AChR) induce loss of functional receptors at the neuromuscular junction. Germinal centers present in MG hyperplastic thymus contain activated B cells spontaneously producing anti-human AChR (anti-huAChR) Ab in vitro. To access the anti-huAChR repertoire, phage display Fab libraries of thymic lymphocytes were constructed from two MG patients. Four Fabs highly specific for huAChR were isolated that bind to determinants in or near the main immunogenic region. These anti-huAChR Fabs showed evidence of significant somatic mutations, supporting the idea that the anti-huAChR Ab response in MG patients is driven by Ag. Two Fabs were able to inhibit up to 90% of donor serum anti-huAChR Abs. Competition with serum anti-huAChR Ab was also observed in unrelated MG patients and indicate that anti-huAChR Fabs bind to epitopes on huAChR recognized by the majority of MG patients. In vitro antigenic modulation studies demonstrated that anti-huAChR Fabs were able to induce AChR loss when cross-linked by an anti-Fab Ab but not as monovalent Fab. Moreover, anti-huAChR Fabs were able to protect against AChR loss by antigenic modulation induced by MG serum Abs, suggesting a potential therapeutic role for these recombinant Fabs in patients with a myasthenic crisis.
    Type of Medium: Online Resource
    ISSN: 0022-1767 , 1550-6606
    URL: Article
    DOI: 10.4049/jimmunol.158.4.1919
    RVK:
    XA 54100
    RVK:
    XA 10000
    Language: English
    Publisher: The American Association of Immunologists
    Publication Date: 1997
    detail.hit.zdb_id: 1475085-5
    Location Call Number Limitation Availability
    BibTip Others were also interested in ...
    Online Resource
  • 3
    Online Resource
    Online Resource
    Sequence analysis of anti-AChR antibodies in experimental autoimmune myasthenia gravis.
    The American Association of Immunologists ; 1995
    In:  The Journal of Immunology Vol. 154, No. 12 ( 1995-06-15), p. 6382-6396
    Details
    In: The Journal of Immunology, The American Association of Immunologists, Vol. 154, No. 12 ( 1995-06-15), p. 6382-6396
    Abstract: Autoantibodies directed against the acetylcholine receptor (AChR) lead to AChR loss and muscular weakness in myasthenia gravis and its experimental model, experimental autoimmune myasthenia gravis (EAMG). The role of different anti-AChR sequences and specificities in the pathogenesis of EAMG was investigated by sequencing a panel of 19 mouse mAbs, previously elicited against Torpedo and human AChR, that bound to at least four different epitope regions. The pathogenicity of eight mAbs that cross-reacted with mouse or rat AChR was tested. EAMG was induced by four mAbs against the main immunogenic region (MIR). Sequence analysis of different anti-AChR specificities showed a large diversity of H and L chain sequences. Highly homologous H chain sequences ( & gt; 90%) were found among some mAbs with similar specificities, whereas highly homologous L chain sequences were not restricted to Abs of a particular fine specificity. Sharing of a highly homologous VH gene or an identical DJH region was observed among three of four pathogenic anti-MIR mAbs, obtained by immunization with AChRs from different species. The VH genes of these three pathogenic mAbs were closely related to PC7183 germline genes indicating that some pathogenic Abs may already be present in the germline repertoire.
    Type of Medium: Online Resource
    ISSN: 0022-1767 , 1550-6606
    URL: Article
    DOI: 10.4049/jimmunol.154.12.6382
    RVK:
    XA 54100
    RVK:
    XA 10000
    Language: English
    Publisher: The American Association of Immunologists
    Publication Date: 1995
    detail.hit.zdb_id: 1475085-5
    Location Call Number Limitation Availability
    BibTip Others were also interested in ...
    Online Resource
  • 4
    Online Resource
    Online Resource
    A monoclonal antibody that induces T cell aggregation reacts with vascular endothelial cells and placental trophoblasts.
    The American Association of Immunologists ; 1986
    In:  The Journal of Immunology Vol. 137, No. 3 ( 1986-08-01), p. 826-829
    Details
    In: The Journal of Immunology, The American Association of Immunologists, Vol. 137, No. 3 ( 1986-08-01), p. 826-829
    Abstract: We have found that a mouse monoclonal antibody (alpha Leu-13) to a 16 kilodalton human lymphocyte surface antigen reacts with vascular endothelial cells as determined by immunoperoxidase staining of frozen tissue sections. In earlier studies, alpha Leu-13 was found to induce purified T cells to aggregate when added to cultures in nanogram concentrations. In the studies reported here, alpha Leu-13 stained vascular endothelial cells of arteries, capillaries, and veins in all organs examined from adults. It also reacted weakly with epithelial cells of proximal tubules of the kidney and with nonkeratinized basal epithelial cells of the cervix and esophagus. When a panel of tissues from a 14-wk-old fetus was examined, alpha Leu-13 was not found to react with endothelial cells of any specimen. However, it did stain medullary thymocytes and placental trophoblasts of this fetus. The implications of these findings to the possible function of the Leu-13 antigen in immune ontogeny are discussed.
    Type of Medium: Online Resource
    ISSN: 0022-1767 , 1550-6606
    URL: Article
    DOI: 10.4049/jimmunol.137.3.826
    RVK:
    XA 54100
    RVK:
    XA 10000
    Language: English
    Publisher: The American Association of Immunologists
    Publication Date: 1986
    detail.hit.zdb_id: 1475085-5
    Location Call Number Limitation Availability
    BibTip Others were also interested in ...
    Online Resource
Close ⊗
This website uses cookies and the analysis tool Matomo. More information can be found here...