HTLV-1, Immune Response and Autoimmunity

Quaresma, Juarez Antônio Simões; Yoshikawa, Gilberto Toshimitsu; Koyama, Roberta Vilela Lopes; Dias, G A S; Fujihara, Satomi; Fuzii, Hellen Thaís

doi:10.3390/v8010005

Cited by 91 publications

(61 citation statements)

References 86 publications

(114 reference statements)

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“…This is in accordance with previous studies that had observed an immunomodulatory response in asymptomatic carriers [62, 70]. Pro-inflammatory cytokines (Th1) are involved in the progression of myelopathy and IFN-γ downregulates the production of IL-4 by Th2 cells [52,70]. We inferred that in asymptomatic individuals, immune responses were modulated to control inflammation by an increased production of IL-4 and IL-10.…”

Section: Discussionsupporting

confidence: 92%

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Cytokine profile and proviral load among Japanese immigrants and non-Japanese infected with HTLV-1 in a non-endemic area of Brazil

et al. 2017

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The lifetime risk of HTLV-1-associated myelopathy/tropical spastic paraparesis (HAM/TSP) development differs among ethnic groups. To better understand these differences, this prospective cohort study was conducted to investigate the cytokine profile and the HTLV-1 proviral load (PVL) in Japanese and non-Japanese populations with HAM/TSP and asymptomatic carriers (ACs). The serum IL-2, IL-4, IL-6, IL-10, IL-17, TNF-α, and IFN-γ levels were quantified using the Cytometric Bead Array in 40 HTLV-1-infected patients (11 HAM/TSP and 29 ACs) and 18 healthy controls (HCs) in Brazil. Among ACs, 15 were Japanese descendants and 14 were non-Japanese. Of 11 patients with HAM/TSP, only one was a Japanese descendant. The HTLV-1 PVL was quantified by real-time PCR. The HTLV-1 PVL was 2.7-fold higher in HAM/TSP patients than ACs. Regardless of the clinical outcome, the PVL was significantly higher in patients younger than 60 years than older patients. The HAM/TSP and ACs had higher IL-10 serum concentrations than that of HCs. The ACs also showed higher IL-6 serum levels than those of HCs. According to age, the IL-10 and IL-6 levels were higher in ACs non-Japanese patients older than 60 years. HAM/TSP patients showed a positive correlation between IL-6 and IL-17 and a negative correlation between the PVL and IL-17 and IFN-γ. In the all ACs, a significant positive correlation was observed between IL-2 and IL-17 and a negative correlation was detected between IL-10 and TNF-α. Only 6.25% of the Japanese patients were symptomatic carriers, compared with 41.67% of the non-Japanese patients. In conclusion, this study showed that high levels of HTLV-1 PVL was intrinsicaly associated with the development of HAM/TSP. A higher HTLV-1 PVL and IL10 levels found in non-Japanese ACs over 60 years old, which compared with the Japanese group depicts that the ethnic background may interfere in the host immune status. More researches also need to be undertaken regarding the host genetic background to better understand the low frequency of HAM/TSP in Japanese HTLV-1-infected individuals.

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Section: Discussionsupporting

confidence: 92%

“…HAM/TSP progression is associated with the HTLV-1 PVL and with an increase in pro-inflammatory cytokines, such as IFN-γ, TNF-α, IL-2, and IL-6 [45,48–52]. The analysis of serum IL-10 demonstrated a higher concentration in patients infected with HTLV-1 (HAM/TSP and ACs) than in healthy controls.…”

Section: Discussionmentioning

confidence: 99%

Cytokine profile and proviral load among Japanese immigrants and non-Japanese infected with HTLV-1 in a non-endemic area of Brazil

et al. 2017

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“…It has been shown that overexpression of the natural p53 inhibitory protein mouse double minute 2 homolog (MDM2) or expression of certain viral proteins upon viral infection, such as human papillomavirus (HPV) E6 and human T-lymphotropic virus 1 (HLTV-1), also lead to inhibition of p53 activity, which has been linked to tumorigenesis [81,82,83,84]. Interestingly, HTLV-1 infection appears to be associated with increased development of autoimmune diseases, including RA, SS, and systemic lupus erythematosus (SLE) [85], although it is yet to be determined whether this HTLV-1-induced chronic inflammation is at least partially resulted by p53 dysfunction in immune cells.…”

Section: Trp53 Dysfunction and Inflammation—the Non-canonical And mentioning

confidence: 99%

Immunomodulatory Function of the Tumor Suppressor p53 in Host Immune Response and the Tumor Microenvironment

Cui

Guo

2016

IJMS

108

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The tumor suppressor p53 is the most frequently mutated gene in human cancers. Most of the mutations are missense leading to loss of p53 function in inducing apoptosis and senescence. In addition to these autonomous effects of p53 inactivation/dysfunction on tumorigenesis, compelling evidence suggests that p53 mutation/inactivation also leads to gain-of-function or activation of non-autonomous pathways, which either directly or indirectly promote tumorigenesis. Experimental and clinical results suggest that p53 dysfunction fuels pro-tumor inflammation and serves as an immunological gain-of-function driver of tumorigenesis via skewing immune landscape of the tumor microenvironment (TME). It is now increasingly appreciated that p53 dysfunction in various cellular compartments of the TME leads to immunosuppression and immune evasion. Although our understanding of the cellular and molecular processes that link p53 activity to host immune regulation is still incomplete, it is clear that activating/reactivating the p53 pathway in the TME also represents a compelling immunological strategy to reverse immunosuppression and enhance antitumor immunity. Here, we review our current understanding of the potential cellular and molecular mechanisms by which p53 participates in immune regulation and discuss how targeting the p53 pathway can be exploited to alter the immunological landscape of tumors for maximizing therapeutic outcome.

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“…A diferencia de lo que ocurre en HIV que destruye los linfocitos CD4, HTLV-1 promueve la proliferación de estas células así como linfocitos CD8 y células NK (19) alterando la función de los linfocitos CD4 a través de una serie de factores de transcripción como la proteína TAX, FOXP3 y el factor nuclear de células T activadas (NFAT), con el desarrollo de respuesta inmune deficiente y autoinmunidad (20).…”

Section: Ventosilla R Y Colunclassified

Histoplasmosis diseminada con síndrome hemofagocítico asociado con infección por HTLV-1. Reporte de caso

Ventosilla

Carpio

2016

Rev Med Hered

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Síndrome hemofagocítico (SH) es un cuadro sistémico severo usualmente fatal, reportado como causa secundaria en adultos. Histoplasmosis ha sido descrita como una de las causas, siempre en pacientes con inmunosupresión. Se presenta el caso de un paciente varón natural de Huánuco con historia de tos y expectoración de dos meses e infiltrado pulmonar intersticial y parenquimal basal derecho con adenopatía mediastinal. Ingresó con fiebre, pancitopenia, alteración de pruebas hepáticas y pruebas de coagulación que cumplía criterios de SH. En el aspirado de médula ósea se observaron inclusiones intracitoplasmáticas en los macrófagos compatibles con Histoplasma capsulatum. La serología para HTLV-1 fue positiva por lo que se analiza el rol de este virus como agente inmunosupresor que condiciona SH secundario a histoplasmosis diseminada.PALABRAS CLAVE: Linfohistiocitosis hemofagocítica, histoplasmosis, virus 1 linfotrópico T humano. (Fuente: DeCS BIREME). SUMMARYThe hemophagocytic syndrome (HS) is a severe systemic illness ultimately fatal associated with underlying conditions. Histoplasmosis has been associated with HS in immunosuppressed patients. We present the case of a male patient from Huanuco with a 2-month history of productive cough and presence of interstitial pulmonary infiltrates, and consolidation in the right lower lobe associated with mediastinal lymphadenopathies on the chest x-ray. The patient presented with fever, pancytopenia and abnormalities in the liver and coagulation tests fulfilling criteria for HS. A bone marrow aspiration showed intracytoplasmic structures within the macrophages compatible with Histoplasma capsulatum. Serology for HTLV-1 was positive. We analyzed the role of HTLV-1 inducing immunosuppression leading to the development of disseminated histoplasmosis and HS.

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HTLV-1, Immune Response and Autoimmunity

Cited by 91 publications

References 86 publications

Cytokine profile and proviral load among Japanese immigrants and non-Japanese infected with HTLV-1 in a non-endemic area of Brazil

Cytokine profile and proviral load among Japanese immigrants and non-Japanese infected with HTLV-1 in a non-endemic area of Brazil

Immunomodulatory Function of the Tumor Suppressor p53 in Host Immune Response and the Tumor Microenvironment

Histoplasmosis diseminada con síndrome hemofagocítico asociado con infección por HTLV-1. Reporte de caso

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