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Mikako Yasuoka,Chikako Tange,Yukiko Nishita,Makiko Tomida,Ryota Watanabe,Hiroshi Shimokata,Rei Otsuka,Masayo Kojima 대한노인병학회 2023 Annals of geriatric medicine and research Vol.27 No.1
Background: This study evaluated the chronological changes in physical and cognitive functions in middle-aged and older adults with and without rheumatoid arthritis (RA). Methods: This population-based case-control longitudinal study included individuals aged 40–79 years at baseline who agreed to participate. We identified 42 participants with RA and randomly selected 84 ageand sex-matched controls. Physical function was assessed according to gait speed, grip strength, and skeletal muscle mass. Cognitive function was assessed based on the information, similarities, picture completion, and digit symbol substitution test scores of the Wechsler Adult Intelligence Scale-Revised Short Form. The general linear mixed models comprised the fixed effects of the intercept, case, age, time in years since baseline, and case×time interaction, which were used to examine longitudinal changes in physical and cognitive functions. Results: Regardless of RA status, grip strength decreased and the picture completion score increased in the group aged <65 years, while skeletal muscle mass index and gait speed decreased in the group aged ≥65 years. The interaction of case×follow-up years for grip strength in the group aged ≥65 years was significant (p=0.03). The decline in grip strength in the control group (slope=-0.45) was greater than that in the RA group (slope=-0.19). Conclusion: Chronological changes in physical and cognitive functions were comparable between participants with and without RA; however, the decline in grip strength in the control group was greater among older adults with RA.
Park, Chang Ook,Fu, Xiujun,Jiang, Xiaodong,Pan, Youdong,Teague, Jessica E.,Collins, Nicholas,Tian, Tian,O'Malley, John T.,Emerson, Ryan O.,Kim, Ji Hye,Jung, Yookyung,Watanabe, Rei,Fuhlbrigge, Robert C Elsevier 2018 The Journal of allergy and clinical immunology Vol.142 No.2
<P><B>Background</B></P> <P> <I>Candida albicans</I> is a dimorphic fungus to which human subjects are exposed early in life, and by adulthood, it is part of the mycobiome of skin and other tissues. Neonatal skin lacks resident memory T (T<SUB>RM</SUB>) cells, but in adults the <I>C albicans</I> skin test is a surrogate for immunocompetence. Young adult mice raised under specific pathogen-free conditions are naive to <I>C albicans</I> and have been shown recently to have an immune system resembling that of neonatal human subjects.</P> <P><B>Objective</B></P> <P>We studied the evolution of the adaptive cutaneous immune response to <I>Candida</I> species.</P> <P><B>Methods</B></P> <P>We examined both human skin T cells and the <I>de novo</I> and memory immune responses in a mouse model of <I>C albicans</I> skin infection.</P> <P><B>Results</B></P> <P>In mice the initial IL-17–producing cells after <I>C albicans</I> infection were dermal γδ T cells, but by day 7, αβ T<SUB>H</SUB>17 effector T cells were predominant. By day 30, the majority of <I>C albicans</I>–reactive IL-17–producing T cells were CD4 T<SUB>RM</SUB> cells. Intravital microscopy showed that CD4 effector T cells were recruited to the site of primary infection and were highly motile 10 days after infection. Between 30 and 90 days after infection, these CD4 T cells became increasingly sessile, acquired expression of CD69 and CD103, and localized to the papillary dermis. These established T<SUB>RM</SUB> cells produced IL-17 on challenge, whereas motile migratory memory T cells did not. T<SUB>RM</SUB> cells rapidly clear an infectious challenge with <I>C albicans</I> more effectively than recirculating T cells, although both populations participate. We found that in normal human skin IL-17–producing CD4<SUP>+</SUP> T<SUB>RM</SUB> cells that responded to <I>C albicans</I> in an MHC class II–restricted fashion could be identified readily.</P> <P><B>Conclusions</B></P> <P>These studies demonstrate that <I>C albicans</I> infection of skin preferentially generates CD4<SUP>+</SUP> IL-17–producing T<SUB>RM</SUB> cells, which mediate durable protective immunity.</P>