Influence of cytokines and immunosuppressive drugs on major histocompatibility complex class I/II expression by human cardiac myocytes in vitro

Wang, Yichong; Herskowitz, Ahvie; Gu, Liqun; Kanter, Kirk R.; Lattouf, Omar M.; Sell, Kenneth W.; Ahmed‐Ansari, A.

doi:10.1016/0198-8859(91)90015-2

Cited by 19 publications

(3 citation statements)

References 32 publications

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“…Cytokines IFN-g, IL-1, IL-4 and TNF-a have been shown to enhance expression of MHC class I antigens in human cardiac myocytes in vitro (Wang et al 1991). Furthermore, an increased expression of MHC class I molecules has been observed in myocardial cells from chronic chagasic patients (Reis et al 1993a).…”

Section: Discussionmentioning

confidence: 99%

Local and systemic cytokine expression during experimental chronic Trypanosoma cruzi infection in a Cebus monkey model

Samudio¹,

Montenegro-James

Kasamatsu³

et al. 1999

Parasite Immunology

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Cebus apella is an acceptable model for chronic chagasic cardiomyopathy (CCC), since it is possible to experimentally induce cardiac lesions after 1 year of Trypanosoma cruzi infection. The T. cruzi Y strain, shown previously to produce CCC in C. apella monkeys, was used to experimentally infect 10 monkeys. Parasitological, serological and clinical parameters were monitored during a 19-month follow-up, and systemic cytokine responses were assessed sequentially in five monkeys selected according to the differential parasitemia pattern exhibited. Ten additional monkeys, infected with the same strain for 5, 10 and 12 years, were analysed cross-sectionally. Three monkeys/time point and one uninfected control animal were sacrificed for gross pathology, histology, presence of parasites, and local cytokine gene expression. Elevated expression of interleukin (IL)-4 was observed throughout the study in monkeys that had persistent, high parasitemias, whereas a high level of interferon (IFN)-gamma was seen in monkeys that controlled parasitemias soon after infection. Chronically infected monkeys expressed a nonpolarized, Th0-type response. Cardiac tissue collected from a monkey that succumbed to acute infection had elevated levels of proinflammatory cytokine [IL-1beta, IL-6, tumour necrosis factor-alpha] and interstitial cell adhesion molecule (ICAM)-1, platelet-derived growth factor (PDGF)-alpha, transforming growth factor (TGF)-beta and IL-10 transcripts. Cytokine production in cardiac tissue of chronically infected monkeys was also characterized by elevated expression of ICAM-1, PDGF-alpha and TGF-beta, which correlated with the detection of T. cruzi DNA by polymerase chain reaction.

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Section: Discussionmentioning

confidence: 99%

Local and systemic cytokine expression during experimental chronic Trypanosoma cruzi infection in a Cebus monkey model

Samudio¹,

Montenegro-James

Kasamatsu³

et al. 1999

Parasite Immunology

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“…Specificity for the regulatory activity of the CPI resides at the tissue level, based on the ligands expressed on tissues that maintain tissue tolerance and inhibit immunopathology. In fact, there is evidence for the expression of the MHC class II, the receptor for LAG-3 in cardiac endothelial cells and endocardial cells in certain disease states in humans and rodents [ 32 – 35 ] as well as in cultured human fetal cardiac myocytes in experimental systems [ 36 ].…”

Section: Introductionmentioning

confidence: 99%

Cardiac morbidity in HIV infection is associated with checkpoint inhibitor LAG-3 on CD4 T cells

et al. 2018

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Recent findings point to a role of Checkpoint Inhibitor (CPI) receptors at the tissue level in immune homeostasis. Here we investigated the role of CPI molecules on immune cells in relation to cardiac function. Participants recruited in Chennai, India consisted of HIV+ ART naive viremic (Gp1 n = 102), HIV+ on ART, virologically suppressed (Gp2, n = 172) and HIV negative healthy controls (Gp3, n = 64). A cross-sectional analysis of cardiac function, arterial resistance and immunologic assessment of CPI expressing T cells was performed. Data indicate that ART naive exhibited cardiac function impairment and greater arterial stiffness than the other groups. Frequencies of CD4+ T cells expressing LAG-3 and PD1 were higher in ART naïve while TIGIT and TIM3 were similar among the patient groups. LAG-3+, PD1+ and dual LAG-3+PD1+ CD4 T cells were inversely correlated with cardiac function and arterial elasticity and directly with arterial stiffness in ART naïve participants and with arterial elasticity in virally suppressed group on ART. We conclude that HIV induced upregulation of LAG-3 singly or in combination with PD1 in immune cells may regulate cardiac health and warrant mechanistic investigations. The implications of these findings have bearing for the potential utility of anti-LAG-3 immunotherapy for cardiac dysfunction in chronic HIV infection.

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“…Because myocyte cultures are derived from cardiac tissue, fibroblast contamination is a universal problem (8,12,14,22,26). It was therefore important to reliably differentiate between myocytes and fibroblasts.…”

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confidence: 99%

Cytopathogenic effect in cardiac myocytes but not in cardiac fibroblasts is correlated with reovirus-induced acute myocarditis

Baty

Sherry

1993

J Virol

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Influence of cytokines and immunosuppressive drugs on major histocompatibility complex class I/II expression by human cardiac myocytes in vitro

Cited by 19 publications

References 32 publications

Local and systemic cytokine expression during experimental chronic Trypanosoma cruzi infection in a Cebus monkey model

Local and systemic cytokine expression during experimental chronic Trypanosoma cruzi infection in a Cebus monkey model

Cardiac morbidity in HIV infection is associated with checkpoint inhibitor LAG-3 on CD4 T cells

Cytopathogenic effect in cardiac myocytes but not in cardiac fibroblasts is correlated with reovirus-induced acute myocarditis

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