Role of Trypanosoma cruzi Trans-sialidase on the Escape from Host Immune Surveillance

John Cunningham virus (JCV) is a member of thePolyomaviridaefamily. It was first isolated from the brain of a patient with Hodgkin disease in 1971, and since then the etiological agent of the progressive multifocal leukoencephalopathy (PML) was considered. Until the human immunodeficiency virus (HIV) pandemic, PML was rare: in fact HIV-induced immunodeficiency is the most common predisposing factor accounting for 85% of all instances of PML. This data led to intense research on JCV infection and resulted in better understanding of epidemiology and clinic-pathologic spectrum. Recently, cases of PML have been observed after the introduction of monoclonal antibodies, such as natalizumab, rituximab, efalizumab, and infliximab, in the treatment of autoimmune disease, underlining the important role of host immunity in PML pathogenesis. In this review current understanding of the JCV infection and the new findings relating to the pathogenesis of PML has been comprehensively revised, focusing our attention on the interaction between the cellular and viral molecular pathways implicated in the JCV infection and the modulating role of host immune surveillance in the viral reactivation from a latent state.

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Deciphering the Role of microRNAs in Regulation of Immune Surveillance, Self-Tolerance and Allograft Transplant Outcome

Current Stem Cell Research & Therapy ◽

10.2174/1574888x11666160201120129 ◽

2018 ◽

Vol 13 (5) ◽

pp. 336-344

Author(s):

Cherry S. Leung ◽

Song Lu ◽

Jiatao Li ◽

William KK Wu ◽

Kathy O. Lui

Keyword(s):

Immune Surveillance ◽

Transplant Outcome ◽

Self Tolerance

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Absence of Bim sensitizes mice to experimental Trypanosoma cruzi infection

Cell Death and Disease ◽

10.1038/s41419-021-03964-6 ◽

2021 ◽

Vol 12 (7) ◽

Author(s):

Marcela Hernández-Torres ◽

Rogério Silva do Nascimento ◽

Monica Cardozo Rebouças ◽

Alexandra Cassado ◽

Kely Catarine Matteucci ◽

...

Keyword(s):

T Cells ◽

Trypanosoma Cruzi ◽

Chagas Disease ◽

Parasite Load ◽

Peritoneal Macrophages ◽

T Cell Response ◽

No Production ◽

Similar Reduction ◽

Ifn Γ

AbstractChagas disease is a life-threatening disorder caused by the protozoan parasite Trypanosoma cruzi. Parasite-specific antibodies, CD8+ T cells, as well as IFN-γ and nitric oxide (NO) are key elements of the adaptive and innate immunity against the extracellular and intracellular forms of the parasite. Bim is a potent pro-apoptotic member of the Bcl-2 family implicated in different aspects of the immune regulation, such as negative selection of self-reactive thymocytes and elimination of antigen-specific T cells at the end of an immune response. Interestingly, the role of Bim during infections remains largely unidentified. To explore the role of Bim in Chagas disease, we infected WT, Bim+/−, Bim−/− mice with trypomastigotes forms of the Y strain of T. cruzi. Strikingly, our data revealed that Bim−/− mice exhibit a delay in the development of parasitemia followed by a deficiency in the control of parasite load in the bloodstream and a decreased survival compared to WT and Bim+/− mice. At the peak of parasitemia, peritoneal macrophages of Bim−/− mice exhibit decreased NO production, which correlated with a decrease in the pro-inflammatory Small Peritoneal Macrophage (SPM) subset. A similar reduction in NO secretion, as well as in the pro-inflammatory cytokines IFN-γ and IL-6, was also observed in Bim−/− splenocytes. Moreover, an impaired anti-T. cruzi CD8+ T-cell response was found in Bim−/− mice at this time point. Taken together, our results suggest that these alterations may contribute to the establishment of a delayed yet enlarged parasitic load observed at day 9 after infection of Bim−/− mice and place Bim as an important protein in the control of T. cruzi infections.

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Switching on the macrophage-mediated suppressor mechanism by tumor cells to evade host immune surveillance.

Proceedings of the National Academy of Sciences ◽

10.1073/pnas.77.7.4265 ◽

1980 ◽

Vol 77 (7) ◽

pp. 4265-4269 ◽

Cited By ~ 30

Author(s):

C. C. Ting ◽

D. Rodrigues

Keyword(s):

Tumor Cells ◽

Immune Surveillance ◽

Suppressor Mechanism ◽

Host Immune Surveillance

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The Impact of Interferon Gamma Receptor Expression on the Mechanism of Escape From Host Immune Surveillance in Hepatocellular Carcinoma

Hepatology ◽

10.1053/jhep.2000.16470 ◽

2000 ◽

Vol 32 (3) ◽

pp. 491-500 ◽

Cited By ~ 34

Author(s):

Mitsuo Nagao ◽

Yoshiyuki Nakajima ◽

Hiromichi Kanehiro ◽

Michiyoshi Hisanaga ◽

Yukio Aomatsu ◽

...

Keyword(s):

Hepatocellular Carcinoma ◽

Interferon Gamma ◽

Immune Surveillance ◽

Receptor Expression ◽

Gamma Receptor ◽

The Impact ◽

Host Immune Surveillance

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Impact of Temozolomide on Immune Response during Malignant Glioma Chemotherapy

Clinical and Developmental Immunology ◽

10.1155/2012/831090 ◽

2012 ◽

Vol 2012 ◽

pp. 1-7 ◽

Cited By ~ 63

Author(s):

Sadhak Sengupta ◽

Jaclyn Marrinan ◽

Caroline Frishman ◽

Prakash Sampath

Keyword(s):

Immune Response ◽

Malignant Glioma ◽

Dna Methyltransferase ◽

Opportunistic Infections ◽

Immune Surveillance ◽

Drug Resistant ◽

Methylguanine Dna Methyltransferase ◽

Drug Resistant Mutation ◽

Resistant Mutation

Malignant glioma, or glioblastoma, is the most common and lethal form of brain tumor with a median survival time of 15 months. The established therapeutic regimen includes a tripartite therapy of surgical resection followed by radiation and temozolomide (TMZ) chemotherapy, concurrently with radiation and then as an adjuvant. TMZ, a DNA alkylating agent, is the most successful antiglioma drug and has added several months to the life expectancy of malignant glioma patients. However, TMZ is also responsible for inducing lymphopenia and myelosuppression in malignant glioma patients undergoing chemotherapy. Although TMZ-induced lymphopenia has been attributed to facilitate antitumor vaccination studies by inducing passive immune response, in general lymphopenic conditions have been associated with poor immune surveillance leading to opportunistic infections in glioma patients, as well as disrupting active antiglioma immune response by depleting both T and NK cells. Deletion of O6-methylguanine-DNA-methyltransferase (MGMT) activity, a DNA repair enzyme, by temozolomide has been determined to be the cause of lymphopenia. Drug-resistant mutation of the MGMT protein has been shown to render chemoprotection against TMZ. The immune modulating role of TMZ during glioma chemotherapy and possible mechanisms to establish a strong TMZ-resistant immune response have been discussed.

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