Expressão de antígenos MHC classe I e de células CD4 e CD8 na polimiosite e dermatomiosite

Graça, Carla; Kouyoumdjian, João Aris

doi:10.1016/j.rbr.2014.10.005

Cited by 6 publications

(3 citation statements)

References 14 publications

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“…In physiological conditions, the levels of MHC molecules in muscle cells are not detectable. However, both MHC-I and II have been reported to be expressed in myofibers upon chronic inflammation (such as in polymyositis) (Graca and Kouyoumdjian, 2015). In vitro , human myoblasts and myotubes can express MHC classic molecules (HLA-DR), either constitutively or after coculture with IFN-γ.…”

Section: Introductionmentioning

confidence: 99%

The IRE1α Arm of UPR Regulates Muscle Cells Immune Characters by Restraining p38 MAPK Activation

Gu¹,

Huang²,

Xiao³

et al. 2019

Front. Physiol.

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Skeletal muscle repair and systemic inflammation/immune responses are linked to endoplasmic reticulum stress (ER stress) pathways in myopathic muscle, and muscle cells play an active role in muscular immune reactions by exhibiting immunological characteristics under persistent proinflammation stimuli. Whether ER stress affects the intrinsic immunological capacities of myocytes in the inflammatory milieu, as it does to immune cells, and which arms of the unfolded protein response (UPR) mainly participate in these processes remain mostly unknown. We investigated this issue and showed that inflammatory stimuli can induce the activation of the protein kinase R (PKR)-like endoplasmic reticulum kinase (PERK) and inositol-requiring enzyme 1α (IRE1α) arms of the UPR in myocytes both in vivo and in vitro. UPR stressor administration reversed the increased IFN-γ-induced expression of the MHC-II molecule H2-Ea, the MHC-I molecule H-2Kb, toll-like receptor 3 (TLR3) and some proinflammatory myokines in differentiated primary myotubes in vitro. However, further IRE1α inhibition thoroughly corrected the trend in the UPR stressor-triggered suppression of immunobiological molecules. In IFN-γ-treated myotubes, dramatic p38 MAPK activation was observed under IRE1α inhibitory conditions, and the pharmacological inhibition of p38 reversed the immune molecule upregulation induced by IRE1α inhibition. In parallel, our coculturing system verified that the ovalbumin (OVA) antigen presentation ability of inflamed myotubes to OT-I T cells was enhanced by IRE1α inhibition, but was attenuated by further p38 inhibition. Thus, the present findings demonstrated that p38 MAPK contributes greatly to IRE1α arm-dependent immunobiological suppression in myocytes under inflammatory stress conditions.

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Section: Introductionmentioning

confidence: 99%

The IRE1α Arm of UPR Regulates Muscle Cells Immune Characters by Restraining p38 MAPK Activation

Gu¹,

Huang²,

Xiao³

et al. 2019

Front. Physiol.

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“…MHC I presents peptides on the cell surface for CD8 T-cell recognition. Because healthy and unperturbed skeletal muscle normally expresses low levels of MHC I ( Wiendl et al, 2005 ; Graca and Kouyoumdjian, 2015 ), these data suggest that upon contraction-induced injury, skeletal muscle may up regulate MHC I and communicate with the CD8 T-cells. The function of these T-cells and whether they were detrimental, beneficial or passive observers to the muscle damage/repair process following contraction-induced damage is not known.…”

Section: Do T-cells Respond To Contraction-induced Muscle Damage?mentioning

confidence: 94%

“…Dystrophic features of dysphyrlin-deficient muscle were greatly reduced with T-cell depletion ( Farini et al, 2012 ). T-cells are implicated in muscle cytotoxicity in idiopathic inflammatory myopathy conditions ( Johnson et al, 1972 ; De Paepe et al, 2005 ; Choi et al, 2009 ; Graca and Kouyoumdjian, 2015 ; Huang et al, 2015 ; Limongi, 2015 ). Recently, T-cells were found to accumulate in the muscle of high fat-fed mice, and were instrumental in the development of insulin insensitivity ( Khan et al, 2014 , 2015 ).…”

Section: T-cells In Muscle Health and Diseasementioning

confidence: 99%

The Role of T Lymphocytes in Skeletal Muscle Repair From Traumatic and Contraction-Induced Injury

Deyhle

Hyldahl

2018

Front. Physiol.

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Skeletal muscle is prone to damage from a range of stimuli, and initiates a robust repair process that requires the participation of immune cells. Among the more well characterized immune cells involved in muscle repair are those of the myeloid lineage, including neutrophils, macrophages, monocytes, and eosinophils. More recently, studies have begun to elucidate the role of the lymphoid-derived immune cells, most notably T lymphocytes (T-cells), in the complex processes of muscle repair. Though T-cells have been traditionally been associated with pathological degeneration of skeletal muscle in disease, recent studies show that T-cells are instrumental in the repair/regeneration process following severe muscle damage in mice. Furthermore, a few studies using basic immunohistochemical assays have shown that T-cells accumulate in human skeletal muscle in the days following contraction-induced muscle damage. The functional significance of T-cells in the repair and adaptation process following contraction-induce muscle damage remains uncertain, and is an active area of intense investigation. This mini-review summarizes recent findings on the involvement of T-cells in skeletal muscle repair.

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Inflammatory Myopathies

Salih

2020

Clinical Child Neurology

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Expressão de antígenos MHC classe I e de células CD4 e CD8 na polimiosite e dermatomiosite

Abstract: MCH-I antigens expression and CD4 positivity might add to strong diagnostic suspicion of PM/DM. No cellular infiltration was observed in 14.3% of such cases.

Cited by 6 publications

References 14 publications

The IRE1α Arm of UPR Regulates Muscle Cells Immune Characters by Restraining p38 MAPK Activation

The IRE1α Arm of UPR Regulates Muscle Cells Immune Characters by Restraining p38 MAPK Activation

The Role of T Lymphocytes in Skeletal Muscle Repair From Traumatic and Contraction-Induced Injury

Inflammatory Myopathies

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