minka breloer (0000-0001-6199-4908)

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Career progression
08.2007 until today
Group leader of the laboratory "helminth immunology" at the Bernhard Nocht Institute for Tropical Medicine
Major Topic: Nematode infections in mice: immune response and immune modulation
02.2002 - 07.2007
Senior Postdoc at the Department of Immunology, Bernhard Nocht Institute for Tropical Medicine
Major Topic: Characterization of the immunological function of the transmembrane protein CD83
01.2002 - 11.2002
Parental leave
08.1999 - 12.2001
Junior Postdoc at the Department of Immunology, Bernhard Nocht Institute for Tropical Medicine
Major Topic: Immune stimulatory functions of autologous HSP60

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Bernhard-Nocht-Institut für Tropenmedizin: Hamburg, Hamburg, DE

2007-08-01 to present | Group Leader "Helminth Immunology" (Immunology)

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minka breloer

https://orcid.org/0000-0001-6199-4908

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Biography

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Employment (1)

Bernhard-Nocht-Institut für Tropenmedizin: Hamburg, Hamburg, DE

Education and qualifications (3)

University of Hamburg: Hamburg, Hamburg, DE

University Hamburg/Bernhard Nocht Institute for Tropical Medicine: Hamburg, DE

University Hamburg: Hamburg, DE

Funding (7)

Hybride Chancen und Herrausforderungen von neuen genomischen Kombinationen

Control and eradication of migrating parasitic nematode larvae by innate effector cells

Modulation of cellular and humoral immune response to third party antigens in nematode-infected mice

Modulation der zellulären und humoralen Immunantwort gegen unbeteiligte Modellantigene in nematodeninfizierten Mäusen

Analysis of Host-Parasite Cross-Talk based on the Bovine Model for Human Onchocerciasis, Onchocerca ochengi

Hitzeschock Protein 60 als immunologischer Signalverstärker

Antigen-spezifische und Antigen-unabhängige Aktivierung von murinen T-Lymphozyten

Works (50 of 74)

Strongyloides questions—a research agenda for the future

Strongyloides ratti infection in mice: immune response and immune modulation

Filarial infections compromise influenza vaccination efficacy: Lessons from the mouse

Corrigendum: Eosinophils and Neutrophils Eliminate Migrating Strongyloides ratti Larvae at the Site of Infection in the Context of Extracellular DNA Trap Formation (Front. Immunol., (2021), 12, 715766, 10.3389/fimmu.2021.715766)

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

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

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

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

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

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

Helminth Infections Suppress the Efficacy of Vaccination against Seasonal Influenza

Rbpj expression in regulatory T cells is critical for restraining TH2 responses

Basophils Are Dispensable for the Control of a Filarial Infection

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

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

Th2/1 hybrid cells occurring in murine and human Strongyloidiasis share effector functions of Th1 cells

Mucosal mast cells are indispensable for the timely termination of Strongyloides ratti infection.

Strongyloides infection in rodents: immune response and immune regulation.

Erratum: Corrigendum to “Functional characterization and immune recognition of the extracellular superoxide dismutase from the human pathogenic parasite Onchocerca volvulus (OvEC-SOD)” (Acta Tropica (2012) 124(1) (15–26))

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

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

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

Immune recognition of Onchocerca volvulus proteins in the human host and animal models of onchocerciasis.

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

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

Heat shock protein 60: an endogenous inducer of dopaminergic cell death in Parkinson disease.

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

Immunization with Brugia malayi Hsp70 protects mice against Litomosoides sigmodontis challenge infection.

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

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

Comparative analysis of macrophage migration inhibitory factors (MIFs) from the parasitic nematode Onchocerca volvulus and the free-living nematode Caenorhabditis elegans.

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

Functional characterization and immune recognition of the extracellular superoxide dismutase from the human pathogenic parasite Onchocerca volvulus (OvEC-SOD).

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

Efficient control of Plasmodium yoelii infection in BALB/c and C57BL/6 mice with pre-existing Strongyloides ratti infection.

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

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.

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

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

Efficient control of Leishmania and Strongyloides despite partial suppression of nematode-induced Th2 response in co-infected mice.

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 induces transient nematode-specific Th2 response and reciprocal suppression of IFN-gamma production in mice.

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

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

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

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

CD83 expression in CD4+ T cells modulates inflammation and autoimmunity.

CD83 regulates lymphocyte maturation, activation and homeostasis.

Peer review (1 review for 1 publication/grant)