Short communication Autoimmunity and longevity: Presence of antinuclear antibodies is not associated with the rate of inflammation or mortality in nonagenarians M. Hurme a,b, * , S. Korkki a , T. Lehtima ¨ki c,b , P.J. Karhunen d,b , M. Jylha ¨ e , A. Hervonen e , M. Pertovaara a,f a Department of Microbiology and Immunology, University of Tampere Medical School, Finland b The Laboratory Centre, Tampere University Hospital, Finland c Department of Clinical Chemistry, University of Tampere Medical School, Finland d Department of Forensic Medicine, University of Tampere Medical School, Finland e Laboratory of Gerontology, Tampere School of Public Health, Finland f Department of Internal Medicine, Tampere University Hospital, Finland Received 15 December 2006; received in revised form 8 February 2007; accepted 13 March 2007 Available online 18 March 2007 Abstract There are reports demonstrating elevated levels of autoantibodies in elderly people. We now analyzed whether the strong inflammatory response associated with aging is interrelated with the production of autoantibodies, antinuclear antibodies (ANA). In a cohort of 284 nonagenarians the rate of ANA positivity was 12.3%, which is significantly ( p < 0.001) higher than that in the middle-aged controls (2.8%). The mortality data of this cohort was collected after a 4-year follow-up. The ANA positivity at the age of 90 did not have any effect on the rate of survival, or on the levels of serum markers of inflammation. # 2007 Elsevier Ireland Ltd. All rights reserved. Keywords: Longevity; Inflammation; Autoimmunity There are many studies demonstrating that the blood levels of several markers of inflammation are increased in elderly individuals and that this increase is associated with shortening of the remaining lifespan (reviewed in Bruunsgaard et al., 2001). However, the factors causing this inflammatory response are still largely unknown. In contrast to the increased rate of inflammation (or innate immunity) the adaptive T cell immunity is clearly weakened (reviewed in Pawelec et al., 2005). The exact mechanism of this defective T cell response is unknown, but it may be due to a relative deficiency of naı ¨ve T cells (reviewed in Pawelec et al., 2005) or to the increased number of the CD4 + CD25 + FOXP3 + T regulatory cells (Gregg et al., 2005). Regardless of the defective immune response, imunosenes- cence, the prevalence of autoantibodies is increased in aged individuals (Xavier et al., 1995, Ioannidis et al., 2003). One reason for this could simply be the catabolic state often associated with aging, which could increase destruction of cells and tissues, thus leading to release of intracellular autoantigens. One of the major mechanisms for clearance of dying, apoptotic cells in the body is phagocytosis assisted by acute phase proteins, such as the pentraxin C-reactive protein (CRP) (reviewed in Kravitz et al., 2005). If this clearance mechanism at the apoptotic stage is defective, cells become necrotic and are able to induce a strong inflammatory response and also an immune response against cellular ‘‘self’’ antigens. Based on this mechanism, it could be hypothesized that excessive release of autoantigens in the elderly would contribute to the rate of inflammation. It could even be the primary cause for it. To examine this interrelationship we now analyzed the presence of ANA in our cohort of nonagenarians and correlated it to mortality in a 4-year follow-up as well as to the levels of different markers of inflammation. The population-based cohort of 284 nonagenarians (217 females and 67 males) analyzed has been described in detail www.elsevier.com/locate/mechagedev Mechanisms of Ageing and Development 128 (2007) 407–408 * Corresponding author at: Department of Microbiology and Immunology, University of Tampere Medical School, FIN-33014 Tampere, Finland. Tel.: +358 3 35516652. E-mail address: mikko.hurme@uta.fi (M. Hurme). 0047-6374/$ – see front matter # 2007 Elsevier Ireland Ltd. All rights reserved. doi:10.1016/j.mad.2007.03.001