Among the age-associated changes in the immune system, the most evident is the decrease in proliferative responses of lymphocytes to mitogenic stimuli, which is accompanied by the loss of cytokine network homeostasis. Chronic low-grade inflammatory stress, termed as sterile inflammation, is also observed during aging. In chronologically and prematurely aging mice, cohabitation with adult animals for two months favored improvements in several immune functions. This study aimed to determine whether cohabitation could restore several cytokine networks, improve lymphoproliferative responses to mitogens, and diminish sterile inflammation. Chronologically old mice (76 ± 4 weeks) and prematurely aging mice (33 ± 4 weeks) (PAM and TH-HZ) were cohabited with adults (without premature aging) for two months. Subsequently, lymphoproliferation in both basal (unstimulated) conditions and in the presence of mitogenic stimuli lipopolysaccharide A (LPS) or concanavalin A (ConA) was analyzed in cultures of peritoneal leukocytes for 48 h. Cytokine secretions (IL-1β, TNF-α, IL-6, IL-10, and IL-17) in these cultures were also evaluated. The results showed that cohabitation restored the levels of these cytokines in old and prematurely aging mice and improved the subsequent lymphoproliferative responses. In addition, this social strategy diminished sterile inflammation and decreased inflammatory stress in unstimulated conditions. Therefore, this strategy seems to be capable of restoring the relevant immune function of lymphocytes and reducing the inflammatory stress, which are the improvements required for an adequate immune response.

在免疫系统与年龄相关的变化中，最明显的是淋巴细胞对有丝分裂刺激的增殖反应减少，这伴随着细胞因子网络稳态的丧失。在衰老过程中也观察到慢性低度炎症应激，称为无菌炎症。在按时间顺序和过早衰老的小鼠中，与成年动物同居两个月有利于改善几种免疫功能。本研究旨在确定同居是否可以恢复多个细胞因子网络，改善对有丝分裂原的淋巴增殖反应，并减少无菌性炎症。按时间顺序排列的老小鼠（76 ± 4 周）和过早衰老小鼠（33 ± 4 周）（PAM 和 TH-HZ）与成年人（没有过早衰老）同居两个月。随后，在腹膜白细胞培养物中分析基础（未刺激）条件和有丝分裂刺激物脂多糖 A (LPS) 或刀豆球蛋白 A (ConA) 存在下的淋巴增殖 48 小时。还评估了这些培养物中的细胞因子分泌物（IL-1β、TNF-α、IL-6、IL-10 和 IL-17）。结果表明，同居恢复了老年和过早衰老小鼠体内这些细胞因子的水平，并改善了随后的淋巴增殖反应。此外，这种社交策略减少了无菌炎症并减少了未受刺激条件下的炎症压力。因此，该策略似乎能够恢复淋巴细胞的相关免疫功能并减少炎症应激，这是充分免疫反应所需的改进。