Galit Alter

Human immunodeficiency virus (HIV)-specific effector CD8 T cell activity in patients with primary HIV infection.

HIV-1-specific cytotoxicity is preferentially mediated by a subset of CD8(+) T cells producing both interferon-gamma and tumor necrosis factor-alpha.

Loss of HIV-1-specific CD8+ T cell proliferation after acute HIV-1 infection and restoration by vaccine-induced HIV-1-specific CD4+ T cells.

Increased natural killer cell activity in viremic HIV-1 infection.

Assessment of longitudinal changes in HIV-specific effector activity in subjects undergoing untreated primary HIV infection.

CD107a as a functional marker for the identification of natural killer cell activity.

Human immunodeficiency virus (HIV)-specific gamma interferon secretion directed against all expressed HIV genes: relationship to rate of CD4 decline.

The majority of currently circulating human immunodeficiency virus type 1 clade B viruses fail to prime cytotoxic T-lymphocyte responses against an otherwise immunodominant HLA-A2-restricted epitope: implications for vaccine design.

Sequential deregulation of NK cell subset distribution and function starting in acute HIV-1 infection.

High degree of inter-clade cross-reactivity of HIV-1-specific T cell responses at the single peptide level.

De novo generation of escape variant-specific CD8+ T-cell responses following cytotoxic T-lymphocyte escape in chronic human immunodeficiency virus type 1 infection.

Consistent effects of TSG101 genetic variability on multiple outcomes of exposure to human immunodeficiency virus type 1.

Low perforin and elevated SHIP-1 expression is associated with functional anergy of natural killer cells in chronic HIV-1 infection.

Immunological and virological impact of highly active antiretroviral therapy initiated during acute HIV-1 infection.

NK cell function in HIV-1 infection.

HLA Alleles Associated with Delayed Progression to AIDS Contribute Strongly to the Initial CD8(+) T Cell Response against HIV-1.

Evolution of innate and adaptive effector cell functions during acute HIV-1 infection.

Recognition of a defined region within p24 gag by CD8+ T cells during primary human immunodeficiency virus type 1 infection in individuals expressing protective HLA class I alleles.

MyD88-dependent immune activation mediated by human immunodeficiency virus type 1-encoded Toll-like receptor ligands.

Single-stranded RNA derived from HIV-1 serves as a potent activator of NK cells.

Detection of KIR3DS1 on the cell surface of peripheral blood NK cells facilitates identification of a novel null allele and assessment of KIR3DS1 expression during HIV-1 infection.

Differential natural killer cell-mediated inhibition of HIV-1 replication based on distinct KIR/HLA subtypes.

Rapid ex vivo isolation and long-term culture of human Th17 cells.

Upregulation of PD-L1 on monocytes and dendritic cells by HIV-1 derived TLR ligands.

Novel KIR3DL1 alleles and their expression levels on NK cells: convergent evolution of KIR3DL1 phenotype variation?

Antigen load and viral sequence diversification determine the functional profile of HIV-1-specific CD8+ T cells.

Ligand-independent exhaustion of killer immunoglobulin-like receptor-positive CD8+ T cells in human immunodeficiency virus type 1 infection.

Rapid loss of dendritic cell and monocyte responses to TLR ligands following venipuncture.

Type 2 Bias of T cells expanded from the blood of melanoma patients switched to type 1 by IL-12p70 mRNA-transfected dendritic cells.

Protective HLA class I alleles that restrict acute-phase CD8+ T-cell responses are associated with viral escape mutations located in highly conserved regions of human immunodeficiency virus type 1.

Report on the AIDS Vaccine 2008 Conference.

Biology of plasmacytoid dendritic cells and natural killer cells in HIV-1 infection.

HLA class I subtype-dependent expansion of KIR3DS1+ and KIR3DL1+ NK cells during acute human immunodeficiency virus type 1 infection.

Matrix metalloprotease inhibitors restore impaired NK cell-mediated antibody-dependent cellular cytotoxicity in human immunodeficiency virus type 1 infection.

Sex differences in the Toll-like receptor-mediated response of plasmacytoid dendritic cells to HIV-1.

Challenges facing young investigators.

Perspective natural killer cells: bridging innate and adaptive immunity?

Alterations in natural killer cell receptor profiles during HIV type 1 disease progression among chronically infected South African adults.

IL-10 induces aberrant deletion of dendritic cells by natural killer cells in the context of HIV infection.

MHC class I chain-related protein A shedding in chronic HIV-1 infection is associated with profound NK cell dysfunction.

The humoral response to HIV-1: new insights, renewed focus.

Determinants of protection among HIV‐exposed seronegative persons: an overview.

Comprehensive analysis of virus-specific T-cells provides clues for the failure of therapeutic immunization with ALVAC-HIV vaccine.

Reduced frequencies of NKp30+NKp46+, CD161+, and NKG2D+ NK cells in acute HCV infection may predict viral clearance.

A robust, high-throughput assay to determine the phagocytic activity of clinical antibody samples.

Expansion of 2B4+ natural killer (NK) cells and decrease in NKp46+ NK cells in response to influenza.

Characteristics of the earliest cross-neutralizing antibody response to HIV-1.

Natural killer cells in spontaneous control of HIV infection.

Mutiny or scrutiny: NK cell modulation of DC function in HIV-1 infection.

KIR polymorphisms modulate peptide-dependent binding to an MHC class I ligand with a Bw6 motif.

Decreased Fc receptor expression on innate immune cells is associated with impaired antibody-mediated cellular phagocytic activity in chronically HIV-1 infected individuals.

Early viral replication in lymph nodes provides HIV with a means by which to escape NK-cell-mediated control.

HIV-1 adaptation to NK-cell-mediated immune pressure.

KIR/HLA: genetic clues for a role of NK cells in the control of HIV.

Emerging Concepts on the Role of Innate Immunity in the Prevention and Control of HIV Infection.

Copy number variation of KIR genes influences HIV-1 control.