Senescent cells release inflammatory signals called SASP that normally recruit immune cells for clearance, but aging weakens this surveillance system. When immune clearance fails, accumulated senescent cells maintain chronic inflammation that damages tissues and promotes fibrosis, metabolic dysfunction, and cancer progression. Critically, immune cells themselves can become senescent, creating destructive feedback loops where compromised immunity allows more senescent cells to persist, which further weakens immune function. This bidirectional deterioration represents a fundamental mechanism driving multiple age-related pathologies simultaneously. The finding helps explain why aging involves systemic decline rather than isolated organ failures. Therapeutically, this opens several intervention points: enhancing immune-mediated clearance of senescent cells, blocking inflammatory SASP signals, or rejuvenating aged immune systems. The senescence-immunity axis may be more targetable than senescence alone, since restoring immune surveillance could theoretically break the self-reinforcing cycles. However, the complexity of these interactions suggests that successful interventions will require sophisticated approaches that enhance beneficial immune responses while dampening harmful inflammation. This framework positions immune system restoration as equally important as direct senolytic therapies for healthy aging.