Figure 1. A depiction of the known effects of SnCs and SASP on different cell types and tissues, and how they are relevant to the immune system. SnCs possess altered morphology and surface markers and usually fail to perform the tasks of their non-senescence counterparts. This makes them the dysfunctional units of a tissue which can impede normal functions such as, immune cell priming and transmigration. MMPs produced by SnCs can modify the surrounding matrix and alter the microarchitecture of the lymphoid organs. As these organs are precisely organized into zones with specialized functions, such micro-architectural alterations can lead to dysfunction. SASP produced by SnCs can act as a chemoattractant to immune cells which can lead to unresolved chronic inflammation in tissues. SASP by itself can be inflammatory which can adversely impact neighboring cells. This chronic unresolved inflammation can lead to pathological conditions like fibrosis and neoplasia. SASP-mediated signaling and ROS-mediated oxidative stress can impair clonogenicity and functionality of HSCs, immune cells and other supporting cells of the immune system. SnCs and SASP can alter the expression profile of supporting cells leading to the dysregulation of homing signals required for proper localization of immune cells, and survival factors required for the endurance of certain immune cells. SnCs, by means of SASP, can influence the cell fate of differentiating cells and in some cases, cause the accumulation of adipocytes in the lymphoid organs. Abbreviations: SnC: Senescent cell; SASP: Senescence associated secretory phenotype; MMPs: Matrix metalloproteases; ROS: Reactive Oxygen Species; HSC: Hematopoietic stem cell.