Human myoblasts as antigen presenting cells

Goebels, Norbert; Michaelis, Dorothea; Wekerle, Hartmut; Hohlfeld, Reinhard

doi:10.1016/0165-5728(91)90335-5

Cited by 53 publications

(37 citation statements)

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“…Opinion is split over whether transfected muscle cells can present the encoded antigen directly to the immune system [16][17][18][19][20], the antigens are secreted by the transfected muscle cells, then taken up and presented by resident or circulating professional APC [9][10][11][12]15], or whether transfected APC directly present the endogenously derived peptides to T cells [14,15]. Evidence supporting each of these alternatives has been advanced, and the immune response elicited in vivo may result from the synergistic integration of these diverse mechanisms.…”

Section: Discussionmentioning

confidence: 99%

“…It has been widely reported that facultative APC, such as human myoblast cells [17,21], Schwann cells [28,29], microvascular smooth muscle cells [30], pigment epithelial cell in the retina [31,32], and endothelial cells [33,34] can present MHC class II-restricted epitopes to CD4 T cells after stimulation with IFN-+ . The ability of IFN-+ to convert facultative into professional APC indicates that, under a cytokine environment provided by an inflammatory reaction, these cell types may play a role in initiating, amplifying, or sustaining local immune reactions.…”

Section: Discussionmentioning

confidence: 99%

“…IFN-+ secreted by inflammatory cells induces the expression of MHC class II and co-stimulatory molecules on myocytes [16][17][18][19][20]. Therefore, we studied the mechanism leading to a local inflammatory reaction (as source of IFN-+ ) within the muscle fiber upon i. m. administration of plasmid DNA.…”

Section: Cpg Motifs Of Dna Vaccines Induce Local Inflammation Which mentioning

confidence: 99%

“…CpG motifs have immunomodulatory effects in vivo by stimulating CD4 T, NK, monocytes, dendritic, and B cells (present in the muscle-infiltrating cells) to secrete cytokines such as IFN-+ , IL-12 and IL-6 [22][23][24], and IFN-+ induces MHC class II expression in myocytes [16][17][18][19][20].…”

Section: Mhc Class II Expression On Myocytes Is Induced By Ifn-q Secrmentioning

confidence: 99%

“…Under certain conditions, such as stimulation with IFN-+ , myocytes can express MHC class II and co-stimulatory molecules required for the priming of CD4 T cells [16][17][18][19][20]. Furthermore, myocytes have been shown to function as APC, particularly in pathological conditions such as dermatomyositis and polymyositis where muscle cells from affected patients induced the activation of muscle-reactive specific T cells [21].…”

Section: Introductionmentioning

confidence: 99%

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CpG motifs of DNA vaccines induce the expression of chemokines and MHC class II molecules on myocytes

et al. 2001

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Section: Cpg Motifs Of Dna Vaccines Induce Local Inflammation Which mentioning

confidence: 99%

Section: Mhc Class II Expression On Myocytes Is Induced By Ifn-q Secrmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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CpG motifs of DNA vaccines induce the expression of chemokines and MHC class II molecules on myocytes

et al. 2001

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Immune and myodegenerative pathomechanisms in inclusion body myositis

Keller

Schmidt

Lünemann

2017

Ann Clin Transl Neurol

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Inclusion Body Myositis (IBM) is a relatively common acquired inflammatory myopathy in patients above 50 years of age. Pathological hallmarks of IBM are intramyofiber protein inclusions and endomysial inflammation, indicating that both myodegenerative and inflammatory mechanisms contribute to its pathogenesis. Impaired protein degradation by the autophagic machinery, which regulates innate and adaptive immune responses, in skeletal muscle fibers has recently been identified as a potential key pathomechanism in IBM. Immunotherapies, which are successfully used for treating other inflammatory myopathies lack efficacy in IBM and so far no effective treatment is available. Thus, a better understanding of the mechanistic pathways underlying progressive muscle weakness and atrophy in IBM is crucial in identifying novel promising targets for therapeutic intervention. Here, we discuss recent insights into the pathomechanistic network of mutually dependent inflammatory and degenerative events during IBM.

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Expression of intercellular adhesion molecule‐1 by myofibers in mdx mice

et al. 2015

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Introduction We investigated the extent to which intercellular adhesion molecule-1 (ICAM-1), a critical protein of the inflammatory response, is expressed in skeletal muscles of mdx mice (a murine model of Duchenne muscular dystrophy). Methods Muscles were collected from control and mdx mice at 2–24 weeks of age and analyzed for ICAM-1 expression by means of Western blot and immunofluorescence. Results Western blot revealed higher expression of ICAM-1 in mdx compared with control muscles through 24 weeks of age. In contrast to control muscles, ICAM-1 was expressed on the membrane of damaged, regenerating, and normal myofibers of mdx mice. CD11b+ myeloid cells also expressed ICAM-1 in mdx muscles, and CD11b+ cells were closely associated with the membrane of myofibers expressing ICAM-1. Conclusions These findings support a paradigm in which ICAM-1 and its localization to myofibers in muscles of mdx mice contributes to the dystrophic pathology.

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Human myoblasts as antigen presenting cells

Cited by 53 publications

References 0 publications

CpG motifs of DNA vaccines induce the expression of chemokines and MHC class II molecules on myocytes

CpG motifs of DNA vaccines induce the expression of chemokines and MHC class II molecules on myocytes

Immune and myodegenerative pathomechanisms in inclusion body myositis

Expression of intercellular adhesion molecule‐1 by myofibers in mdx mice

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