Experimental Gerontology - $5 might not allow the identification of significant differences, these data seem to suggest that the genetic component of the longevity achievement may be important for women too. However, it has to be remembered that the expression of the IFN-y gene may be subject to direct hormonal control. In a transient expression assay, the steroid 17B-estradiol was shown to markedly increase the activity of the IFN- promoter in lymphoid cells that expressed the appropriate hormone receptor. This effect is mediated by sequences in the 2AM5/-flanking region of the gene. Hormonal regulation of this pleiotropic cytokine has been suggested to account in part for the ability of estrogens to potentiate many types of immune responses and for the disproportionate susceptibility of women to immune-inflammatory diseases (Verthelyi and Klinman, .///:5). Thus, it has to be taken into account that gene variants representing genetic advantage for one gender might not automatically be relevant for the other gender in terms of successful or unsuccessful ageing. 

The polymorphism might have functional consequences for transcription of the human IFN-y gene. Therefore, the polymorphism might directly influence the level of IFN-y production associated with the microsatellite marker (Pravica et al., .///:5). The activity reflected increased circulating levels of pro-inflammatory cytokines and acute phase proteins (Franceschi et al., .///(24)0; Bruunsgaard et al., .//,:5). Systemic consequences include a pattern of changes attributed to chronic inflammatory diseases or frailty (Ershler and Keller, .///:5). Epidemiological studies suggest that chronic low-grade inflammation in ageing promotes an atherogenic profile and is related to age-associated inflammatory diseases and enhanced mortality risk (Harris et al., .;;;0; Bruunsgaard et al., .//,:5). 

Accordingly, polymorphic alleles of inflammatory cytokines, determining changes in cytokine production, play an important role in age-related inflammatory diseases and unsuccessful ageing (Grimaldi et al., .///0; Hobson and Ralston, .//,0; McCusker et al., .//,:5). Moreover, it has been recently reported thatThe magnitude of the spontaneous release of interferon-y (IFN-y) and tumor necrosis factor-a from cells is negatively correlated with the decrease of the cognitive function score of Alzheimer's disease patients (Solerte et al., 2000). This provides evidence that the complex puzzle of genetic and environmental factors involved in the control of life span expectancy in humans may be influenced by cytokine gene polymorphisms, which can help individuate a network of trans-interactive genes capable of influencing the type and strength of responses to environmental stressors, ultimately conditioning individual life expectancy. Subjects with a pro-inflammatory profile have a negative outcome, making it sensible that possession of the +874A allele, known to be associated with low IFN-y production, is significantly increased in centenarians with a pro-inflammatory status (Candore et al., 2002). These data strengthen the suggestion that pro-inflammatory status characteristics of ageing may be detrimental for successful ageing, and concomitantly suggest that tight control of the inflammatory status may contribute to survival of extreme ages. 

Several findings point out that gender is a major variable in the genetics of longevity and suggest the working hypothesis that men rely more upon genetics than women in order to attain longevity (Franceschi et al., 2000). The present data indicate instead that the +874 IFN-y allele distribution is different in centenarian women with respect to controls, but not in centenarian men. 

Acknowledgements: ST, Rome; MP, Immunogenetics of Longevity; SN, coordinated by Prof. A. Caruso; and VN from the Ministry of Health and Projects Immunological parameters related to age and Pharmacogenomics of Alzheimer's Disease, from the Sicilian government Breast Cancer and Immune Response. This work was also performed under the aegis of an EU programme called ImAginE. 

References: 
Candore G et al., 2002. Immunogenetics, 54: 734-738. 
Franceschi C et al., 2000. Aging Clin Exp Res, 12: 77-84.The original text appears to be a mix of scientific terms and phrases that are not well-structured or formatted, making it difficult to understand the intended meaning. Here's the processed text with corrections:

Interferon-gamma (IFN-gamma) gene: deep sequencing reveals an absolute negative correlation with laryngeal squamous cell carcinoma. Microsatellite markers are indicative of high IFN-gamma gene expression. Production of IFN-gamma and TNF-alpha from natural killer (NK) cells is associated with abnormal NK cell reactivity and cognitive impairment in Alzheimer's disease. Annals of the New York Academy of Sciences. Genetic polymorphism in the first intron of the human IFN-gamma gene is associated with lung allograft fibrosis. Immunology News.

Immunomodulatory properties of interferon-gamma. The immunology of exceptional individuals: lessons from centenarians. Inflamm-aging: an evolutionary perspective on immunosenescence. Aging and pro-inflammatory cytokines: a current opinion on hematological diseases.

Estrogen regulates the IFN-gamma promoter. The immunogenetics of longevity is relevant to the histocompatibility complex polymorphism and control of human longevity.

Age-associated increased interleukin gene expression, late-life diseases, and frailty are regulated by estrogen. Immunology Today.

HLA, aging, and longevity: a critical reappraisal. Immunogenetics of longevity: data review from literature.

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