Fig. 2
From: Aging and respiratory viral infection: from acute morbidity to chronic sequelae
Aging is associate with dysfunctional anti-viral immunity. a, b Impaired innate immunity against respiratory virus infection. a The aged hosts have decreased capacity to clear foreign bodies including the virus particles. The production of key anti-viral cytokines like Type I IFN is also abrogated with progressing age. Besides the cytokine production, reduced AM self-renewal also hinders anti-viral response because of AMs’ ability to prevent the ATI cells from the virus infection and to phagocytose virus and virus-infected cells. Additionally, the dysfunction of NK cell infiltration and function also contributes to the defect. b DCs also contribute to the malfunctional anti-viral response in the elderly. Aged lung has increased PGD2 level, which abrogates cDC’ migration to the lymph node, where they prime T cell responses. Moreover, both cDCs and pDCs have reduced production of Type I and /or type III IFNs upon viral stimulation. c–e Aging compromises the adaptive immunity against virus infection. c Aging is associated with decline in the total size of naïve T cell pool, accompanied by accumulation of memory-like CD8 T cell and terminally differentiated CD8+ effector cell (TEMRA) population. Both the populations display reduced repertoire diversity, which limits the effective cellular response in the aged host towards new virus infection. d Dysfunctional CD4 T cell help contribute to the impaired humoral response in the aged host. Activated CD4 T cells have a fate choice biased towards TFR instead of TFH. And they displayed reduce migration towards the Germinal Center. e Age-associated B cells accumulate with progressing age, accompanied by suboptimal humoral response following respiratory viral infection and/or vaccination