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Pathologic T cell immunosenescence drives the development of age-associated autoimmune peripheral neuropathy

McCarthy, E. C.; Seyedsadr, M.; Bang, M. F.; Pham, C. L. H.; Bustillos, C.; Salladay-Perez, I.; Whitmire, J. K.; Lechner, M. G.; Shieh, P.; Covarrubias, A. J.; Su, M. A.

2026-01-08 immunology
10.64898/2026.01.07.698250 bioRxiv
Show abstract

While certain autoimmune conditions occur commonly in the young, others are more frequent in the aged. A striking example is chronic inflammatory demyelinating polyneuropathy (CIDP), an autoimmune disease of peripheral nerves that occurs at a peak decade of onset of 70-79 years. How aging predisposes to autoimmunity, however, remains unclear. In CIDP patients, we identified an expanded population of T cells that exhibit hallmark senescence features, including increased SA-{beta}Gal activity and higher CDKN1A expression. These senescence associated T cells express multiple senescence associated secretory phenotype (SASP) factors (IFN-{gamma}, TNF-, TGF-{beta}, IL21, Spp1) and demonstrated an enhanced capacity for inciting neuropathy in a CIDP mouse model. Notably, SASP suppression by a clinically available senomorphic therapy dampened senescence features in peripheral nerves and protected mice against neuropathy. Together, these findings delineate a key role for T cells exhibiting a pro-inflammatory SASP in predisposing to age-associated autoimmune disease.

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