Publications by authors named "M Nouri-Shirazi"

Current methodologies for assessing vaccine effectiveness and longevity primarily center on measuring vaccine-induced neutralizing antibodies in serum or plasma. However, these methods overlook additional parameters such as the presence of memory B cells, even as antibody levels wane, and the pivotal role played by memory T cells in shaping antigen-specific memory B cell responses. Several studies have employed a combination of polyclonal activators, such as CpG and R848, along with various cytokines to provoke the recall of memory B cells from peripheral blood mononuclear cells (PBMCs) into antibody-secreting cells (ASCs).

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Organ shortage continues to be the forefront of problems facing clinical transplantation. Although xenografts serve as a promising alternative, its success is contingent upon further investigation into the mechanisms of cell-mediated xenograft rejection. Here, we explored the direct and indirect contribution of human immune cells in xenorecognition using human and murine in vitro coculture systems.

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It is known that cigarette smoke compromises the immune system and increases the risk of vaccine-preventable diseases. We reported that nicotine, the immunosuppressive component of cigarette smoke, disrupts the functional properties of DC and DC crosstalk with NK cells, which is pivotal in the initiation of immune responses to vaccines. We also showed that select TLR agonists could reduce the degrading effects of nicotine on DC-NK mediated immune responses in vitro.

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Background: Toll-like receptor (TLR) 7 agonists are effective candidates for Th1 immune adjuvants, which compensate for the insufficient Th1 immune responses induced by traditional adjuvants. This effect is currently dependent on TLR7-mediated induction of dendritic cell (DC) maturation and increased IL-12 production.

Methods: In vivo, we intraperitoneally injected TLR agonists with OVA, and LNs were collected for detection.

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The magnitude of immune responses to vaccination is a critical factor in determining protection from disease. It is known that cigarette smoke dampens the immune system and increases the risk of vaccine-preventable diseases. We reported that nicotine, the immunosuppressive component of cigarette smoke, disrupts the differentiation and functional properties of DC, which are pivotal in the initiation of immune response to vaccines.

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