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Instead we post into the void for ~1 like (often from an expert on said topic) and this keeps us motivated

Humans have abundant autoantibodies and anti-viral antibodies that are stable with time via PhIP-Seq. This includes antibodies to critical human peptide hormones in a new library we just built CDI Labs.

Real benefit could be “distract” more than “boost” based on same data. Reminding immunity to pay MORE attention to an extant chronic infection will reduce attacks on inevitable age-acquired neoantigens in the aged brain.

“How to make antibodies bind things” will be solved long before “why to make antibodies bind things.” Each human immune system is a natural experiment teaching us “what” antibodies can do. To use, pair seromic data with acquired chronic phenotypes derived from them.

And autoantibodies blocking these signals exist… and oxidative stress created by modern diets would often transform these signals with AGEs as neoantigens / up rates of autoabs blocking satiation on modern diets…

Anti-satiation autoantibodies. Likely vs a PTM-modified peptide hormone created in the modern dietary environment. Far more exposed than develop the immune event.

Damage mechanism via direct infectious damage or chronic mimicry-induced autoimmunity?

LUCA had DNA to RNA to ribosome; can’t be earliest life. RNA world is great and all but if we know anything about microbes they don’t go extinct. You’d have to sterilize the planet. Earlier forms either haven’t been identified (possible) or were never here (panspermia).

Everything about this (especially increasing effect size with maternal age) screams “immunologic phenomenon.” Imagine there’s an autoantibody associated with ‘male/female’ birth skew.

New #JITC article: Therapeutic potential of T-cell receptor targeting the HLA-A*11:01-restricted KRASG12V neoantigen without cross-recognition of the self-antigen RAB7B in solid tumors bit.ly/44IMZ5H