Various Types of Acquired Resistance to Experimental ‘Allergic’ Encephalomyelitis

Svet-Moldavsky, George J.; Svet-Moldavskaya, I. A.; Raffkina, L. I.

doi:10.1038/1841552a0

Cited by 24 publications

(5 citation statements)

References 5 publications

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“…Lumsden (17), Svet-M oldavskaya and Svet-M oldavsky (18) and K ies a n d A lvord (19) succeeded in preventing experimental aller gic encephalomyelitis by prior injection of a non-encephalitogenic mixture containing oil and tubercle bacilli. They suggested as possible explanations for this suppression of disease either the "resistance of peripheral type" (20), or interference of the Koch phenomenon (19).…”

Section: Histological Changes In Lymph Xodes Produced By Injection Omentioning

confidence: 99%

Suppression of Experimental Allergic Thyroiditis, Delayed Sensitivity and Antibody Formation to Homologous Thyroglobulin in Guinea-Pigs by Prior Injection of Adjuvant

Janković¹

1962

Int Arch Allergy Immunol

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Section: Histological Changes In Lymph Xodes Produced By Injection Omentioning

confidence: 99%

Suppression of Experimental Allergic Thyroiditis, Delayed Sensitivity and Antibody Formation to Homologous Thyroglobulin in Guinea-Pigs by Prior Injection of Adjuvant

Janković¹

1962

Int Arch Allergy Immunol

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“…Animals which have recovered from EAE are resistant to the induction of a second attack (69, 70). Resistance induced by injection of nerve‐tissue and adjuvant (17) was an expected finding.…”

Section: Clinical Supportive Evidencementioning

confidence: 72%

“…Resistance induced by injection of nerve‐tissue and adjuvant (17) was an expected finding. However, it has been observed that the injection of tissues other than nerve (e.g., adrenal) with adjuvant (72), or of adjuvant alone (70), results in resistance to the subsequent induction of EAE. This hypothesis can explain these curious, hitherto unexplained, observations.…”

Section: Clinical Supportive Evidencementioning

confidence: 99%

Autosensitization Cell Membrane Diseases: A Unifying Concept of Autoimmune Diseases, Collagen Diseases, Neuromyopathies and Cancer

Makari

1972

J American Geriatrics Society

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It is proposed that the term "autosensitization cell membrane (ACM) diseases" be applied to a conglomerate of disorders in which there apparently is a state of autosensitization to common glycolipid plasma membrane (GPM) antigens. Except for cancer, all the other ACM diseases may be the result of this autosensitization to GPM antigens. These disorders are subdivided on the basis of the cell source of GPM, whether from erythrocytes as in autoimmune haemolytic anaemia, from endothelial cells as in collagen diseases, from epithelial cells as in organ-specific immune diseases, or from nerve cells as in neuromyopathies. In cancer, two types of autosensitization occur. The first is autosensitization t o GPM originating from damaged normal cells adjoining cancer cells. The second is autosensitization to cancer-specific tumour polysaccharide substance (TPS) antigens originating in the cancer cells themselves. Evidence for this hypothesis is presented. THE COMMON ANTIGENA glycolipid substance present as a component of certain cell membranes is apparently the common antigen that gives rise to auto-

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“…Upregulation of TGF-β1 in astrocytes characterizes the early phases of MS and EAE, and promotes brain infiltration by myelin oligodendrocyte glycoprotein- (MOG-) specific pro-inflammatory CD4 cells [ 34 ]. Interestingly, administration of complete Freund adjuvant (CFA), a potent inducer of TGF-β1 in astrocytes [ 34 ] before induction of EAE protects from the disease [ 35 ]. These observations suggest that TGF-β1 produced by astrocytes might also exert a protective role in EAE.…”

Section: Discussionmentioning

confidence: 99%

Ectonucleotidase activity and immunosuppression in astrocyte-CD4 T cell bidirectional signaling

et al. 2016

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Astrocytes play a crucial role in neuroinflammation as part of the glia limitans, which regulates infiltration of the brain parenchyma by leukocytes. The signaling pathways and molecular events, which result from the interaction of activated T cells with astrocytes are poorly defined. Here we show that astrocytes promote the expression and enzymatic activity of CD39 and CD73 ectonucleotidases in recently activated CD4 cells by a contact dependent mechanism that is independent of T cell receptor interaction with class II major histocompatibility complex (MHC). Transforming growth factor-β (TGF-β) is robustly upregulated and sufficient to promote ectonucleotidases expression. T cell adhesion to astrocyte results in differentiation to an immunosuppressive phenotype defined by expression of the transcription factor Rorγt, which characterizes the CD4 T helper 17 subset. CD39 activity in T cells in turn inhibits spontaneous calcium oscillations in astrocytes that correlated with enhanced and reduced transcription of CCL2 chemokine and Sonic hedgehog (Shh), respectively. We hypothesize this TCR-independent interaction promote an immunosuppressive program in T cells to control possible brain injury by deregulated T cell activation during neuroinflammation. On the other hand, the increased secretion of CCL2 with concomitant reduction of Shh might promote leukocytes extravasation into the brain parenchyma.

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Various Types of Acquired Resistance to Experimental ‘Allergic’ Encephalomyelitis

Cited by 24 publications

References 5 publications

Suppression of Experimental Allergic Thyroiditis, Delayed Sensitivity and Antibody Formation to Homologous Thyroglobulin in Guinea-Pigs by Prior Injection of Adjuvant

Suppression of Experimental Allergic Thyroiditis, Delayed Sensitivity and Antibody Formation to Homologous Thyroglobulin in Guinea-Pigs by Prior Injection of Adjuvant

Autosensitization Cell Membrane Diseases: A Unifying Concept of Autoimmune Diseases, Collagen Diseases, Neuromyopathies and Cancer

Ectonucleotidase activity and immunosuppression in astrocyte-CD4 T cell bidirectional signaling

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