Publications by authors named "Joan Chapman"

Natural killer (NK) cells bridge the interface between innate and adaptive immunity and are implicated in the control of herpes simplex virus 2 (HSV-2) infection. In subjects infected with human immunodeficiency virus 1 (HIV-1), the critical impact of the innate immune response on disease progression has recently come into focus. Higher numbers of NK cells are associated with lower HIV-1 plasma viraemia.

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Clinical events such as heart attack and stroke can be caused by the rupture of atherosclerotic plaques in artery walls. Computational modeling is often used to better understand atherosclerotic disease progression to identify "vulnerable" plaques (i.e.

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Article Synopsis
  • Chronic HIV-1 infection leads to T cells losing their ability to fight the virus, and a new type of these weak T cells has been found that shows a protein called Tim-3 on their surface.
  • In people with HIV-1, nearly half of their CD8(+) T cells express Tim-3, which is much more than in people without HIV-1.
  • Targeting and blocking the Tim-3 pathway in T cells can help them work better and produce important signals to fight the virus, making it a promising idea for new treatments.
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Background: CD4+CD25high regulatory T (TReg) cells modulate antigen-specific T cell responses, and can suppress anti-viral immunity. In HTLV-1 infection, a selective decrease in the function of TReg cell mediated HTLV-1-tax inhibition of FOXP3 expression has been described. The purpose of this study was to assess the frequency and phenotype of TReg cells in HTLV-1 asymptomatic carriers and in HTLV-1-associated neurological disease (HAM/TSP) patients, and to correlate with measures of T cell activation.

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IL-17 is proinflammatory cytokine secreted by a unique CD4+ T (Th17) cell subset and proposed to play a role in host defense. We hypothesized that Th17 cells are lost in HIV-1 infection. HIV-1-infected children with plasma viremia below 50 copies/ml had IL-17 production, whereas those with detectable viremia had minimal secretion.

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Recent studies indicate that innate immunity in influenza virus infection is an area of substantial importance for our understanding of influenza virus pathogenesis, yet our knowledge of the mechanisms controlling innate immunity remains limited. Further delineation of the roles of NK cells and innate immunity in viral infection may have important implications for the development of improved influenza virus vaccines. In this study, we evaluated the phenotype and function of NK and T lymphocytes, as well as influenza virus-specific immunoglobulin G production, prior to and following vaccination with the routinely administered trivalent influenza virus vaccine.

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Human endogenous retroviruses (HERVs) are remnants of ancient infectious agents that have integrated into the human genome. Under normal circumstances, HERVs are functionally defective or controlled by host factors. In HIV-1-infected individuals, intracellular defense mechanisms are compromised.

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Mycobacterium tuberculosis (MTB) is a leading cause of mortality worldwide from an infectious agent. Natural killer T (NKT) cells recognize mycobacterial antigens and contribute to anti-MTB immunity in mouse models. NKT cells were measured in subjects with pulmonary tuberculosis, MTB-exposed individuals, and healthy controls.

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Background: Antigen-specific CTL responses are thought to play a central role in containment of HIV-1 infection, but no consistent correlation has been found between the magnitude and/or breadth of response and viral load changes during disease progression.

Methods And Findings: We undertook a detailed investigation of longitudinal CTL responses and HIV-1 evolution beginning with primary infection in 11 untreated HLA-A2 positive individuals. A subset of patients developed broad responses, which selected for consensus B epitope variants in Gag, Pol, and Nef, suggesting CTL-induced adaptation of HIV-1 at the population level.

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Background: In utero transmission of HIV-1 occurs on average in only 3%-15% of HIV-1-exposed neonates born to mothers not on antiretroviral drug therapy. Thus, despite potential exposure, the majority of infants remain uninfected. Weak HIV-1-specific T-cell responses have been detected in children exposed to HIV-1, and potentially contribute to protection against infection.

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The enzyme-linked immunospot (ELISPOT) assay is a highly sensitive and reproducible method for quantifying T cell-mediated immune responses, and has been used to measure antigen-specific responses post-vaccination. While there are several advantages of the ELISPOT assay for use in field settings for large-scale vaccination trials, blood draw volumes are often limited, and the number of antigen-specific responses that can be measured is constrained by the limited cell number. We reasoned that it should be possible to salvage and rescue viable cells from a completed ELISPOT assay post-incubation, to use for further experimentation.

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