Minka Breloer

Macrophages as main inducers of IFN-gamma in T cells following administration of human and mouse heat shock protein 60.

Purification of the eucaryotic heat-shock proteins Hsp70 and gp96.

Lipopolysaccharide-free heat shock protein 60 activates T cells.

Transgenic expression of a CD83-immunoglobulin fusion protein impairs the development of immune-competent CD4-positive T cells.

Synergistic and differential modulation of immune responses by Hsp60 and lipopolysaccharide.

CD83 is a regulator of murine B cell function in vivo.

Heat shock proteins: linking danger and pathogen recognition.

CD83 modulates B cell function in vitro: increased IL-10 and reduced Ig secretion by CD83Tg B cells.

Hsp60-mediated T cell stimulation is independent of TLR4 and IL-12.

CD83 regulates lymphocyte maturation, activation and homeostasis.

CD83 regulates splenic B cell maturation and peripheral B cell homeostasis.

CD83 on murine APC does not function as a costimulatory receptor for T cells.

Engagement of CD83 on B cells modulates B cell function in vivo.

Heat shock protein 60 (HSP60) stimulates neutrophil effector functions.

Activated T cells induce rapid CD83 expression on B cells by engagement of CD40.

Strongyloides ratti infection induces expansion of Foxp3+ regulatory T cells that interfere with immune response and parasite clearance in BALB/c mice.

Strongyloides ratti infection modulates B and T cell responses to third party antigens.

Pathogenic nematodes suppress humoral responses to third-party antigens in vivo by IL-10-mediated interference with Th cell function.

Nematode-induced interference with the anti-Plasmodium CD8+ T-cell response can be overcome by optimizing antigen administration.

Vaccination with Strongyloides ratti heat shock protein 60 increases susceptibility to challenge infection by induction of Th1 response.

Passive immunization with a monoclonal IgM antibody specific for Strongyloides ratti HSP60 protects mice against challenge infection.

T-cell-derived, but not B-cell-derived, IL-10 suppresses antigen-specific T-cell responses in Litomosoides sigmodontis-infected mice.

Nematode-derived proteins suppress proliferation and cytokine production of antigen-specific T cells via induction of cell death.

Foxp3⁺ regulatory T cells delay expulsion of intestinal nematodes by suppression of IL-9-driven mast cell activation in BALB/c but not in C57BL/6 mice.

Nematode-induced interference with vaccination efficacy targets follicular T helper cell induction and is preserved after termination of infection.

Cutting Edge: the BTLA-HVEM regulatory pathway interferes with protective immunity to intestinal Helminth infection.

Protein kinase CK2 enables regulatory T cells to suppress excessive TH2 responses in vivo.

Anti-CD83 promotes IgG1 isotype switch in marginal zone B cells in response to TI-2 antigen.

Litomosoides sigmodontis induces TGF-β receptor responsive, IL-10-producing T cells that suppress bystander T-cell proliferation in mice.

Strongyloides infection in rodents: immune response and immune regulation.

Corrigendum to "Functional characterization and immune recognition of the extracellular superoxide dismutase from the human pathogenic parasite Onchocerca volvulus (OvEC-SOD)" [Acta Trop. 124 (2012) 15-26].

Filariae-Retrovirus Co-infection in Mice is Associated with Suppressed Virus-Specific IgG Immune Response and Higher Viral Loads.

Interleukin-9 promotes early mast cell-mediated expulsion of Strongyloides ratti but is dispensable for generation of protective memory.

Basophils are dispensable for the establishment of protective adaptive immunity against primary and challenge infection with the intestinal helminth parasite Strongyloides ratti.

Rbpj expression in regulatory T cells is critical for restraining T2 responses.

Basophils Are Dispensable for the Control of a Filarial Infection.

Helminth Infections Suppress the Efficacy of Vaccination against Seasonal Influenza.

Limited role of mast cells during infection with the parasitic nematode Litomosoides sigmodontis.

IL-33 facilitates rapid expulsion of the parasitic nematode Strongyloides ratti from the intestine via ILC2- and IL-9-driven mast cell activation.

Elucidating different pattern of immunoregulation in BALB/c and C57BL/6 mice and their F1 progeny.

Eosinophils and Neutrophils Eliminate Migrating Larvae at the Site of Infection in the Context of Extracellular DNA Trap Formation.

A Combination of Deworming and Prime-Boost Vaccination Regimen Restores Efficacy of Vaccination Against Influenza in Helminth-Infected Mice.

Pre-existing helminth infection impairs the efficacy of adjuvanted influenza vaccination in mice.

Corrigendum: Eosinophils and Neutrophils Eliminate Migrating Larvae at the Site of Infection in the Context of Extracellular DNA Trap Formation.

Author Correction: Toll like receptor 4 mediates cell death in a mouse MPTP model of Parkinson disease.

Filarial infections compromise influenza vaccination efficacy: Lessons from the mouse.

IRF4 is required for migration of CD4 T cells to the intestine but not for Th2 and Th17 cell maintenance.

Retinoic acid drives intestine-specific adaptation of effector ILC2s originating from distant sites.

infection in mice: immune response and immune modulation.

questions-a research agenda for the future.

Evaluating alternative compounds for strongyloidiasis therapy: Novel insights from larval migration inhibition test.

The C-type lectin receptor MINCLE interferes with eosinophil function and protective intestinal immunity in Strongyloides ratti-infected mice.