Immunosenescence and lymphomagenesis

Abstract

One of the most important determinants of aging-related changes is a complex biological process emerged recently and called “immunosenescence”. Immunosenescence refers to the inability of an aging immune system to produce an appropriate and effective response to challenge. This immune dysregulation may manifest as increased susceptibility to infection, cancer, autoimmune disease, and vaccine failure. At present, the relationship between immunosenescence and lymphoma in elderly patients is not defined in a satisfactory way.This review presents a brief overview of the interplay between aging, cancer and lymphoma, and the key topic of immunosenescence is addressed in the context of two main lymphoma groups, namely Non Hodgkin Lymphoma (NHL) and Hodgkin Lymphoma (HL). Epstein Barr Virus (EBV) plays a central role in the onset of neoplastic lymphoproliferation associated with immunological changes in aging, although the pathophysiology varies vastly among different disease entities. The interaction between immune dysfunction, immunosenescence and Epstein Barr Virus (EBV) infection appears to differ between NHL and HL, as well as between NHL subtypes.

Oxidative-Inflammatory Stress in Immune Cells from Adult Mice with Premature Aging

“…were higher ( p < 0.001) than those from the NPAM and WT, but also from those in PAM ( p < 0.01) and TH-HZ mice ( p < 0.001) (Figure 5B). However, the results of the percentages of stimulation of lymphoproliferation in response to mitogens such as ConA (Figure 5C), a capacity that clearly decreases with age [2,10,37,39,40,47], showed lower values ( p < 0.001) in cells of old animals than in those of adult controls (NPAM and WT). The values obtained in adult PAM and TH-HZ were also lower ( p < 0.01 and p < 0.001, respectively) than those in their corresponding controls and similar to those in old animals in the case of PAM, although higher ( p < 0.05) in the case of TH-HZ mice.…”

Orbital and Eyelid B-Cell Lymphoma: A Multicenter Retrospective Study

“…The old age of patients may indeed play a role in the pathogenesis of OEL. Recent studies have underlined how immunosenescence plays an essential, but poorly defined, role in the development of lymphomas [35]. Furthermore, immunosenescence is associated with a complex dysfunction that increases sensitivity to infections, and some reports have suggested a relationship between age-related immune dysregulation, OEL subtypes and infections [35,36].…”

“…Recent studies have underlined how immunosenescence plays an essential, but poorly defined, role in the development of lymphomas [35]. Furthermore, immunosenescence is associated with a complex dysfunction that increases sensitivity to infections, and some reports have suggested a relationship between age-related immune dysregulation, OEL subtypes and infections [35,36]. In our study, we did not find any statistically significant correlation between presumed risk factors (infection with Helicobacter pylori, Chlamydia psittaci, HBV, HCV or history of rheumatoid arthritis, Sjógren's syndrome or other connective tissue diseases) and recurrence rate, but we recorded a higher incidence of HCV infection in FLs (55.5%) and DLBCLs (38.5%), particularly in those cases with a more diffuse dissemination at the onset (80%).…”

“…No association was detected in our study between the T category and recurrence. The AJCC proposed additional factors recommended just for clinical care: the International Prognostic Index (IPI), tumor cell growth fraction (Ki-67, MIB-1) and lactate dehydrogenase level [ 34 , 35 , 36 , 37 , 38 , 39 , 40 , 41 , 42 , 43 , 44 , 45 , 46 , 47 , 48 , 49 , 50 , 51 , 52 , 53 , 54 , 55 ]. Nonetheless, these factors were not considered in this series as complete data were available only for a small percentage of studied patients.…”

A primer on ageing studies in mice: Considerations, opportunities and limitations

“…There are many factors during ageing that result in an increased susceptibility to disease and the impact of ageing can vary greatly from individual to individual. Pathways affected or phenotypes exacerbated by ageing (reviewed in [1]) include; metabolism [2], telomeres [3,4], mitochondrial function [5,6], increased senescence [7,8], inflammaging [3,9], and immunosenescence [3,10].…”