International Journal of Clinical and Diagnostic Pathology

International Journal of Clinical and Diagnostic Pathology

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Vol. 3 Issue 1 Part D

2020, Vol. 3 Issue 1, Part DPages: 248-251

Phenotype and kinetics of the endogenous pulmonary CD4 T cell response to a primary influenza: A virus infection

Dr. Poonam Sharma, Dr. Pawan Kumar, Dr. Suman Sharma, Dr. Priyadershini Rangari
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ABSTRACT
Background: Viral and bacterial pneumonias are a leading killer of children and adults worldwide. Influenza A virus (IAV) is one of the most common causes of viral pneumonias, infecting up to 20% of the population each year.
Objectives: To provides insight into the specialized subsets present in the influenza A virus-specific CD4 T cell response in the lungs and demonstrates that this response is regulated by pulmonary antigen presenting cells.
Methods: Female BALB/c and C57Bl/6 mice at 8-12 weeks of age for all experiments were used. Age- and weight-matched groups of female C57Bl/6 mice were lightly anesthetized by isoflurane inhalation and infected intra nasally.
Results: A significant increase in the frequency of CD4 T cells producing IFNγ following incubation with peptide-pulsed splenic stimulator DC, compared with CD4 T cells incubated with non-peptide-pulsed splenic stimulator DC.IAV-specific CD4 and CD8 T cells specific for highly conserved epitopes within the internal proteins of IAV can provide hetero subtypic protection. Conclusion: Authors found that IAV and GAS are individually important human pathogens that cause a significant amount of global disease and death. Understanding the immune response to these pathogens is the key to development of better treatments and vaccinations.


International Journal of Clinical and Diagnostic Pathology
How to cite this article:
Dr. Poonam Sharma, Dr. Pawan Kumar, Dr. Suman Sharma, Dr. Priyadershini Rangari. Phenotype and kinetics of the endogenous pulmonary CD4 T cell response to a primary influenza: A virus infection. Int J Clin Diagn Pathol 2020;3(1):248-251. DOI: 10.33545/pathol.2020.v3.i1d.182
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