In contrast to HIV, KIR3DS1 does not influence outcome in HTLV-1 retroviral infection

O’Connor, Geraldine M.; Basatena, Nafisa-Katrin Seich al; Olavarria, Viviana Nilla; MacNamara, Aidan; Vine, Alison M.; Ying, Qi; Hisada, Michie; Galvão–Castro, Bernardo; Asquith, Becca; McVicar, Daniel W.

doi:10.1016/j.humimm.2012.05.006

Cited by 7 publications

(4 citation statements)

References 31 publications

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“…iKIR "rescuing" of activated CD8 + T cells may be particularly important in this setting. Most KIR-HLA genetic associations are not replicated across viral infections, for example, KIR3DS1 with HLA-Bw4 is pro-tective in the context of HIV-1 but not HTLV-1 (56); this is difficult to understand unless a very strong peptide dependence is postulated. In contrast, we report that all iKIRs enhance HLA class I associations in all three persistent virus infections we have studied (HIV-1, HCV, and HTLV-1), which suggests a universality that is often missing from KIR studies.…”

Section: Discussionmentioning

confidence: 99%

Inhibitory killer cell immunoglobulin-like receptors strengthen CD8 ⁺ T cell–mediated control of HIV-1, HCV, and HTLV-1

et al. 2018

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Killer-cell immunoglobulin-like receptors (KIRs) are expressed predominantly on natural killer cells, where they play a key role in the regulation of innate immune responses. Recent studies show that inhibitory KIRs can also impact adaptive T cell-mediated immunity. In mice and in human T cells in vitro, inhibitory KIR ligation enhanced CD8+ T cell survival. To investigate the clinical relevance of these observations, we conducted an extensive immunogenetic analysis of multiple, independent cohorts of HIV-1, hepatitis C virus (HCV) and human T cell leukemia virus (HTLV-1)-infected individuals in conjunction with in vitro assays of T cell survival, analysis of ex vivo KIR expression and mathematical modeling of host-virus dynamics. Our data suggest that functional engagement of inhibitory KIRs enhances the CD8+ T cell response against HIV-1, HCV and HTLV-1 and is a significant determinant of clinical outcome in all three viral infections.

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Section: Discussionmentioning

confidence: 99%

Inhibitory killer cell immunoglobulin-like receptors strengthen CD8 ⁺ T cell–mediated control of HIV-1, HCV, and HTLV-1

et al. 2018

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“…The role of KIR3DS1 has also been investigated in other viral infections such as human T-cell leukemia virus type 1 (HTLV-1), H1N1 influenza A, and hepatitis B virus infection (HBV). While no evidence for the participation of KIR3DS1 in control of HTLV-1 infection was found ( O’Connor et al, 2012 ), carriage of KIR3DS1 and other haplotype B containing KIRs was associated with severe pandemic influenza A (H1N1) 2009 infections ( Aranda-Romo et al, 2012 ). Frequencies of KIR3DS1 as well as KIR2DS1 and KIR2DL5 were furthermore increased in a group of patients who spontaneously recovered from HBV compared to individuals with chronic HBV infection or healthy controls ( Zhi-Ming et al, 2007 ).…”

Section: Role Of the Kir3ds1 In Diseasesmentioning

confidence: 99%

Role of KIR3DS1 in human diseases

Körner¹,

Altfeld²

2012

Front. Immun.

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The function of natural killer (NK) cells is controlled by several activating and inhibitory receptors, including the family of killer-immunoglobulin-like receptors (KIRs). One distinctive feature of KIRs is the extensive number of various haplotypes generated by the gene content within the KIR gene locus as well as by highly polymorphic members of the KIR gene family, namely KIR3DL1/S1. Within the KIR3DL1/S1 gene locus, KIR3DS1 represents a conserved allelic variant and displays other unique features in comparison to the highly polymorphic KIR3DL1 allele. KIR3DS1 is present in all human populations and belongs to the KIR haplotype group B. KIR3DS1 encodes for an activating receptor featuring the characteristic short cytoplasmic tail and a positively charged residue within the transmembrane domain, which allows recruitment of the ITAM-bearing adaptor molecule DAP12. Although HLA class I molecules are thought to represent natural KIR ligands, and HLA-Bw4 molecules serve as ligands for KIR3DL1, the ligand for KIR3DS1 still needs to be identified. Despite the lack of formal evidence for an interaction of KIR3DS1 with HLA-Bw4-I80 or any other HLA class I subtype to date, a growing number of associations between the presence of KIR3DS1 and the outcome of viral infections have been described. Especially, the potential protective role of KIR3DS1 in combination with HLA-Bw4-I80 in the context of HIV-1 infection has been studied intensively. In addition, a number of recent studies have associated the presence or absence of KIR3DS1 with the occurrence and outcome of some malignancies, autoimmune diseases, and graft-versus-host disease (GVHD). In this review, we summarize the present knowledge regarding the characteristics of KIRD3S1 and discuss its role in various human diseases.

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“…In contrast, other studies found no association between polymorphisms in HLA and KIR alleles with HTLV-1 infection. Although KIR3DS1 expression has been associated with host response in HIV infection, KIR3DS1-mediated regulation on HTLV-1 infection does not occur or is ineffective [46]. Likewise, other polymorphisms in the HLA-C and KIR alleles were also not associated with the risk of progressing to HAM [43].…”

Section: Htlv-1 Infected Subjects’ Immunogenetic Profilementioning

confidence: 99%

Influence of Immunogenetic Biomarkers in the Clinical Outcome of HTLV-1 Infected Persons

Vallinoto

Queiroz

et al. 2019

Viruses

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Human T-lymphotropic virus 1, a member of the Retroviridae family, causes a neglected, silent, persistent infection affecting circa 5 to 10 million people around the world, with biology, immune pathology, clinical diseases, epidemiology, and laboratory issues still unsolved. Most of the infected subjects are asymptomatic, but severe clinical disorders appear as a neurodegenerative disease (HTLV-1 associated myelopathy—HAM) or a lymphoprolipherative disorder (Adult T Leukemia/Lymphoma—ATLL) and in other target organs of the human body. HTLV-1 infections are frequently asymptomatic, but there is a large spectrum of diseases that have been described along the years. The mechanisms by which the virus interacts with the host, the different modes of response of the host to the infection, and the immunogenic characteristics of the host are some of the interesting and unanswered questions that may direct the outcome of the disease. The most relevant published results dealing with the genetic variations of the host, the immune response to HTLV-1 infection, and the outcome of the infection are presented herein, including Human Leucocyte Antigen (HLA), Killer Immunoglobulin-like Receptors (KIR), interleukin 6, 10, 28, Fas and Fas ligand, IFN-gamma, TNF-A, and Mannose-binding lectin. In summary, there are still several unmet research needs in the field of useful biomarkers on HTLV-1 pathogenesis.

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In contrast to HIV, KIR3DS1 does not influence outcome in HTLV-1 retroviral infection

Cited by 7 publications

References 31 publications

Inhibitory killer cell immunoglobulin-like receptors strengthen CD8 ⁺ T cell–mediated control of HIV-1, HCV, and HTLV-1

Inhibitory killer cell immunoglobulin-like receptors strengthen CD8 ⁺ T cell–mediated control of HIV-1, HCV, and HTLV-1

Role of KIR3DS1 in human diseases

Influence of Immunogenetic Biomarkers in the Clinical Outcome of HTLV-1 Infected Persons

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In contrast to HIV, KIR3DS1 does not influence outcome in HTLV-1 retroviral infection

Cited by 7 publications

References 31 publications

Inhibitory killer cell immunoglobulin-like receptors strengthen CD8 + T cell–mediated control of HIV-1, HCV, and HTLV-1

Inhibitory killer cell immunoglobulin-like receptors strengthen CD8 + T cell–mediated control of HIV-1, HCV, and HTLV-1

Role of KIR3DS1 in human diseases

Influence of Immunogenetic Biomarkers in the Clinical Outcome of HTLV-1 Infected Persons

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Inhibitory killer cell immunoglobulin-like receptors strengthen CD8 ⁺ T cell–mediated control of HIV-1, HCV, and HTLV-1

Inhibitory killer cell immunoglobulin-like receptors strengthen CD8 ⁺ T cell–mediated control of HIV-1, HCV, and HTLV-1