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Khaleda Rahman Qazi

Researcher at Karolinska University Hospital

Publications -  8
Citations -  1717

Khaleda Rahman Qazi is an academic researcher from Karolinska University Hospital. The author has contributed to research in topics: Microvesicles & T cell. The author has an hindex of 7, co-authored 8 publications receiving 1464 citations. Previous affiliations of Khaleda Rahman Qazi include Karolinska Institutet.

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Exosomes with Immune Modulatory Features Are Present in Human Breast Milk

TL;DR: Functional analysis revealed that the vesicle preparation inhibited anti-CD3-induced IL-2 and IFN-γ production from allogeneic and autologous PBMC incubated with milk vesicles, concluding that human breast milk contains exosomes with the capacity to influence immune responses.
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Antigen-loaded exosomes alone induce Th1-type memory through a B-cell-dependent mechanism.

TL;DR: It is found that B cells are needed for exosomal T-cell stimulation because Bruton tyrosine kinase-deficient mice showed abrogated B- and T- cell responses after OVA-Exo immunization.
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Dendritic Cell-Derived Exosomes Need To Activate Both T and B Cells To Induce Antitumor Immunity

TL;DR: Proper activation of CD4+ T and B cells needs to be considered when designing cancer vaccines to ensure full potential of the treatment.
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Proinflammatory exosomes in bronchoalveolar lavage fluid of patients with sarcoidosis

TL;DR: Results indicate for the first time a role for exosomes in human lung disease with possible contributions to the initiation and progression of inflammation in sarcoidosis and suggest that exosome may be a new potential target for the clinical treatment of lung diseases.
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Nanovesicles from Malassezia sympodialis and host exosomes induce cytokine responses--novel mechanisms for host-microbe interactions in atopic eczema.

TL;DR: Extracellular vesicles from M. sympodialis, dendritic cells and plasma can contribute to cytokine responses in CD14, CD34 depleted and undepleted PBMC of AE patients and HC and have implications for understanding host-microbe interactions in the pathogenesis of AE.