Pandemic H1N1 influenza virus triggers a strong T helper cell response in human nasopharynx-associated lymphoid tissues.
Autor: | Mahallawi WH; Clinical Laboratory Sciences Department, College of Applied Medical Sciences, Taibah University, Madinah, Saudi Arabia., Khabour OF; Department of Medical Laboratory Sciences, Faculty of Applied Medical Sciences, Jordan University of Science and Technology, Irbid, Jordan. |
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Jazyk: | angličtina |
Zdroj: | Saudi journal of biological sciences [Saudi J Biol Sci] 2024 Mar; Vol. 31 (3), pp. 103941. Date of Electronic Publication: 2024 Jan 28. |
DOI: | 10.1016/j.sjbs.2024.103941 |
Abstrakt: | The pH1N1 belongs to influenza A family that is sometimes transmitted to humans via contact with pigs. Human tonsillar immune cells are widely used as in vitro models to study responses to influenza viruses. In the current study, human memory (M) and naïve (N) T cells responses in mononuclear cells of tonsil (TMCs) and peripheral blood (PBMCs) were stimulated by pH1N1/sH1N1, and then stained for estimation of T cells proliferation index. Individuals with an anti-pH1N1 hemagglutination (HA) inhibition (HAI) titer of forty or greater exhibited stronger HA-specific M-CD4 + T cells responses to pH1N1 in TMCs/PBMCs than those with an HAI titer of less than forty (P < 0.01). In addition, a positive correlation was observed between proliferation indices of M-CD4 + T cells induced by exposure to sH1N1/pH1N1 (p < 0.01). Moreover, a strong correlation (p < 0.001) was detected between subjects' age and their HA-specific M-CD4 + T cells induced by pH1N1 exposure, indicating that this response was age-dependent. Finally, stimulation of TMCs with pH1N1-HA resulted in a significant M-CD8 + T cells response (p < 0.05). In conclusion, pH1N1 HA elicits a strong M-CD4 + T cells response in TMCs. Additionally, this response correlates with the response to sH1N1 suggesting cross-reactivity in T cells epitopes directed against HAs of both viral strains. Competing Interests: The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper. (© 2024 The Authors.) |
Databáze: | MEDLINE |
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