Splenic and inguinal lymph node T cells of aged mice respond differently to polyclonal and antigen-specific stimuli☆
References (22)
- et al.
Cell. Immunol
(1988) - et al.
Cell. Immunol
(1991) - et al.
- et al.
Mech. Ageing Dev
(1984) - et al.
Cell. Immunol
(1987) - et al.
Cell. Immunol
(1989) - et al.
Mech. Ageing Dev
(1984) - et al.
Mech. Ageing Dev
(1983) - et al.
Exp. Gerontol
(1991) - et al.
J. Interferon Res
(1985)
Annu. Rev. Gerontol. Geriatr
Cited by (61)
Sex as a confounding factor in the effects of ageing on rat lymph node t cell compartment
2020, Experimental GerontologyCitation Excerpt :In LNs and PB from rats of both sexes, the CD4+/CD8+ T cell ratio decreased with age, but to a greater extent in males. Similar changes were found in murine SLOs (Kirschmann and Murasko, 1992; Arsenović-Ranin et al., 2017) and human blood (Ferguson et al., 1995). Of note, the ageing-related decline in this ratio in humans is considered to be not only a surrogate biomarker of immunosenescence, but also an independent predictor of all-cause mortality (Ferguson et al., 1995).
Strain specificities in influence of ageing on germinal centre reaction to inactivated influenza virus antigens in mice: Sex-based differences
2020, Experimental GerontologyCitation Excerpt :This decline in the number of GC B splenocytes correlated with the age-associated decrease in B-cell activation/proliferation in response to TIV in splenocyte cultures, as shown by Ki-67 staining. This age-related decrease in B-cell activation/proliferation could reflect not only the B cell intrinsic changes occurring with ageing (Frasca et al., 2003), but also, as previously suggested (Kirschmann and Murasko, 1992; Swain et al., 2005), the decline in the capacity of CD4+ T cells to proliferate in response to antigenic stimulation (as shown in TIV-restimulated splenocyte cultures) and thereby to provide optimal help to the B cells. Additionally, the age-related decrease in B cell proliferation may reflect downregulation of CD154 (CD40L), the key molecule providing direct CD4+ T cell-to-B cell communication, due to chronic energy stress in CD4+ T cells occurring with ageing (Eaton et al., 2004; Weyand and Goronzy, 2016; Yu et al., 2012).
Strain specificities in age-related changes in mechanisms promoting and controlling rat spinal cord damage in experimental autoimmune encephalomyelitis
2018, Experimental GerontologyCitation Excerpt :This could reflect the greater frequency of MBP responsive cells in dLNs of aged AO rats, and consequently in dLN cell cultures at the beginning of the restimulation, and/or their greater proliferative response to MBP stimulation. In accordance with some previous studies (Kirschmann and Murasko, 1992; Nikolich-Zugich et al., 2012), the analyses of proliferation of freshly isolated and ConA-stimulated CD8+ T lymphocytes in dLN cell cultures showed age-related decline in their proliferation capacity, which was especially prominent in AO rats. Strain specificities in T lymphocytes proliferation to mitogen (Sydney et al., 2014) and, particularly important, in the age-related changes in their proliferative capacity (Kirschmann and Murasko, 1992) have already been shown.
Strain specificities in cellular and molecular immunopathogenic mechanisms underlying development of experimental autoimmune encephalomyelitis in aged rats
2017, Mechanisms of Ageing and DevelopmentCitation Excerpt :Given that the activated CD4+ T lymphocytes are the main producers of IL-2 (Nelson, 2004), it is highly likely that its production was greater in CD4+ lymphocytes from AO rat dLN cell cultures. The discrepancy between hereby reported findings and those previously obtained in dLN cell cultures from strain-matched young rats (Stojić-Vukanić et al., 2016; Vukmanović et al., 1989), could be reconciled by data indicating that in mice, aging influences CD4+ lymphocyte IL-2 production in a strain-specific manner (Kirschmann and Murasko, 1992; Kubo and Cinader, 1990). To further support the previous notion are data indicating that aging does not affect IL-2 production by CD4+ T lymphocytes from Fischer 344 rats in culture (Holbrook et al., 1989).
Adenosine triphosphate-binding cassette transporter genes in ageing and age-related diseases
2003, Ageing Research Reviews
- ☆
Supported by NIH AG08659.