Anthony Jaworowski

HIV-1 down-modulates gamma signaling chain of Fc gamma R in human macrophages: a possible mechanism for inhibition of phagocytosis.

Defective phagocytosis by human monocyte/macrophages following HIV-1 infection: underlying mechanisms and modulation by adjunctive cytokine therapy.

Human immunodeficiency virus type 1 infection inhibits granulocyte-macrophage colony-stimulating factor-induced activation of STAT5A in human monocyte-derived macrophages.

Phagocytic efficiency of monocytes and macrophages obtained from Sydney blood bank cohort members infected with an attenuated strain of HIV-1.

Low TRBP levels support an innate human immunodeficiency virus type 1 resistance in astrocytes by enhancing the PKR antiviral response.

Phagocytosis stimulates mobilization and shedding of intracellular CD16A in human monocytes and macrophages: inhibition by HIV-1 infection.

The use of growth factors and cytokines to treat opportunistic infections in HIV-1 disease.

Normal CD16 expression and phagocytosis of Mycobacterium avium complex by monocytes from a current cohort of HIV-1-infected patients.

Adverse effects of antiretroviral drugs on HIV-1-infected and -uninfected human monocyte-derived macrophages.

Impaired complement-mediated phagocytosis by HIV type-1-infected human monocyte-derived macrophages involves a cAMP-dependent mechanism.

The mechanism underlying defective Fcgamma receptor-mediated phagocytosis by HIV-1-infected human monocyte-derived macrophages.

The CD16+ monocyte subset is more permissive to infection and preferentially harbors HIV-1 in vivo.

CD16+ monocyte subset preferentially harbors HIV-1 and is expanded in pregnant Malawian women with Plasmodium falciparum malaria and HIV-1 infection.

A novel flow cytometric phagocytosis assay of malaria-infected erythrocytes.

4th International AIDS Society Conference on HIV Pathogenesis, Treatment and Prevention.

Relationship between human immunodeficiency virus type 1 coinfection, anemia, and levels and function of antibodies to variant surface antigens in pregnancy-associated malaria.

Effects of HIV-1 infection in vitro on transendothelial migration by monocytes and monocyte-derived macrophages.

Antibodies to variant surface antigens of Plasmodium falciparum-infected erythrocytes are associated with protection from treatment failure and the development of anemia in pregnancy.

Enhanced monocyte Fc phagocytosis by a homologue of interleukin-10 encoded by human cytomegalovirus.

The macrophage: the intersection between HIV infection and atherosclerosis.

Decreased NK Cell FcRgamma in HIV-1 infected individuals receiving combination antiretroviral therapy: a cross sectional study.

Establishment of HIV-1 latency in resting CD4+ T cells depends on chemokine-induced changes in the actin cytoskeleton.

HIV inhibits early signal transduction events triggered by CD16 cross-linking on NK cells, which are important for antibody-dependent cellular cytotoxicity.

Early events of HIV-1 infection: can signaling be the next therapeutic target?

Differential expression of CD163 on monocyte subsets in healthy and HIV-1 infected individuals.

HIV infection and aging of the innate immune system.

HIV infection induces age-related changes to monocytes and innate immune activation in young men that persist despite combination antiretroviral therapy.

HIV-1 inhibits phagocytosis and inflammatory cytokine responses of human monocyte-derived macrophages to P. falciparum infected erythrocytes.

Endothelial cell activation promotes foam cell formation by monocytes following transendothelial migration in an in vitro model.

Aging is associated with chronic innate immune activation and dysregulation of monocyte phenotype and function.

Anti-HIV-1 antibody-dependent cellular cytotoxicity mediated by hyperimmune bovine colostrum IgG.

Virologically suppressed HIV patients show activation of NK cells and persistent innate immune activation.

Advances in infection and immunity: from bench to bedside.

Opsonization of malaria-infected erythrocytes activates the inflammasome and enhances inflammatory cytokine secretion by human macrophages.

Age-associated changes in monocyte and innate immune activation markers occur more rapidly in HIV infected women.

HIV and co-infections.

Associations between surface markers on blood monocytes and carotid atherosclerosis in HIV-positive individuals.

Increased glucose metabolic activity is associated with CD4+ T-cell activation and depletion during chronic HIV infection.

Peripheral blood mononuclear cells derived from grand multigravidae display a distinct cytokine profile in response to P. falciparum infected erythrocytes.

Opsonic phagocytosis of Plasmodium falciparum merozoites: mechanism in human immunity and a correlate of protection against malaria.

Glucose transporter 1-expressing proinflammatory monocytes are elevated in combination antiretroviral therapy-treated and untreated HIV+ subjects.

Viremic and Virologically Suppressed HIV Infection Increases Age-Related Changes to Monocyte Activation Equivalent to 12 and 4 Years of Aging, Respectively.

Inflammation-induced foam cell formation in chronic inflammatory disease.

An NK Cell Population Lacking FcRγ Is Expanded in Chronically Infected HIV Patients.

CD14(hi)CD16+ monocytes phagocytose antibody-opsonised Plasmodium falciparum infected erythrocytes more efficiently than other monocyte subsets, and require CD16 and complement to do so.

Properties of HIV-1 associated cholesterol in addition to raft formation are important for virus infection.

Monocytes from HIV-infected individuals show impaired cholesterol efflux and increased foam cell formation after transendothelial migration.

Erratum to: CD14 hi CD16+ monocytes phagocytose antibody-opsonised Plasmodium falciparum infected erythrocytes more efficiently than other monocyte subsets, and require CD16 and complement to do so.

Ex vivo foam cell formation is enhanced in monocytes from older individuals by both extrinsic and intrinsic mechanisms.

HIV integration and the establishment of latency in CCL19-treated resting CD4(+) T cells require activation of NF-κB.

Persistence of Activated and Adaptive-Like NK Cells in HIV(+) Individuals despite 2 Years of Suppressive Combination Antiretroviral Therapy.

Dysfunctional HDL from HIV+ individuals promotes monocyte-derived foam cell formation in vitro.

Perturbed CD8(+) T cell immunity across universal influenza epitopes in the elderly.