Role of Innate Immune Cells in the Control of Influenza A Virus Infection
DOI:
https://doi.org/10.55145/ajbms.2026.05.01.016Keywords:
influenza type A virus, innate immunity, and influenza virus controlAbstract
In human immune response against invading viruses, the innate immune system plays a critical role in the early defense towards variable viral infections before the adaptive immune response triggered, particularly against influenza viruses, like with influenza A virus type. Dendritic cells and macrophages are key players in this type of immunity, which is activated to kill infected cells and release antiviral cytokines like interferon-gamma that either reduce the infection or recruit other types of immune cells, like T cells, to the site of infection. The purpose of the study was to look at how innate immune cells contribute to the formation of viral reservoirs and long-term maintenance. Innate immune cells play a critical role in influenza spontaneous control. This study studied previous studies on the Influenza type A Viral infection and who Innate immune cell control this infection. Databases such as Google Scholar and PubMed were investigated. Neutrophils are examples of innate immune cells that can react to infection by phagocytosing virus-infected cells, creating neutrophil extracellular traps (NETs), which are crucial for immobilizing invasive viruses, and releasing inflammatory cytokines. Additionally, macrophages present antigens, phagocytose viruses, and produce cytokines to stimulate additional immune cells, including T cells. By stimulating T-cells, dendritic cells can operate as a mediator to activate the innate and adaptive immune systems. In order to develop treatment strategies aimed at improving basic immune responses and minimizing severe infection, it is crucial to comprehend the distinct roles of each innate immune cell in the defense against influenza.
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Copyright (c) 2026 Marwa Lafta Jabur, Eman A. Muhsin, Shahrazad Ahmed Khalaf

This work is licensed under a Creative Commons Attribution 4.0 International License.



