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Despite the increase in age-related hearing loss (ARHL) prevalence owing to increased population aging, preventive measures against ARHL have not yet been established. The immune system becomes one of the most dysfunctional systems upon aging, and immunosenescence greatly affects homeostasis and promotes systemic aging along with chronic inflammation and oxidative stress. This study aimed to determine whether immuno-rejuvenation procedures can prevent ARHL and have clinical applications as well as to analyze the communication mechanisms between the systemic immune system and the cochlea using a murine model. Lymphocytes from young mice inhibited the progression of ARHL. The method of cryopreserving these lymphocytes and inoculating them at the onset of ARHL suggests their clinical application. Mice that were administered this treatment not only maintained auditory threshold but also avoided spinal ganglion degeneration, cellular immune aging, and nitric oxide production, which causes age-related tissue damage. These findings coincide with our previous strategies against immunosenescence and neuronal aging. Therefore, the manipulation of systemic immune function may contribute not only to the prevention of ARHL but also to the development of novel anti-aging clinical measures, paving the way to healthy longevity with preserved organ function. [Display omitted] • Age-related hearing loss (ARHL) does not have established preventive measures. • Inoculation of cryopreserved lymphocytes from young mice led to immune regeneration. • This immune manipulation inhibited ARHL progression in aged mice. • Cochlear atrophy and oxidative stress were also suppressed in the hosts. • Autologous lymphocyte inoculation may have clinical application in ARHL prevention. [ABSTRACT FROM AUTHOR]

We investigated the association between cellular immunity and age-related hearing loss (ARHL) development using three CD4+ T cell fractions, namely, naturally occurring regulatory T cells (Treg), interleukin 1 receptor type 2-expressing T cells (I1R2), and non-Treg non-I1R2 (nTnI) cells, which comprised Treg and I1R2-deleted CD4+ T cells. Inoculation of the nTnI fraction into a ARHL murine model, not only prevented the development of ARHL and the degeneration of spiral ganglion neurons, but also suppressed serum nitric oxide, a source of oxidative stress. Further investigations on CD4+ T cell fractions could provide novel insights into the prevention of aging, including presbycusis. [Display omitted] • Injections of a lymphoid fraction prevented increasing age-related hearing loss. • This treatment also suppressed cochlear degeneration and serum nitric oxide levels. • Lymphocytes perturbing immune functions were removed from this fraction in advance. • Alterations of the immune system may be effective for anti-aging measures. [ABSTRACT FROM AUTHOR]