Stronger inflammatory/cytotoxic T cell response in women identified by microarray analysis

Hewagama, Anura; Patel, Dipak R.; Yarlagadda, Sushma; Strickland, Faith M.; Richardson, Bruce C.

doi:10.1038/npre.2008.2690.1

Cited by 28 publications

(32 citation statements)

References 2 publications

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“…It has been known for decades that gender has an influence on the function of the immune system, with females generally having a stronger immune response. Gender differences in the immune response are also detectable at transcriptomic levels [24]. Sex steroids, estrogen and testosterone, clearly play a role in driving gender differences in the immune response.…”

Section: Discussionmentioning

confidence: 99%

Transcriptional Analysis Reveals Gender-Specific Changes in the Aging of the Human Immune System

et al. 2013

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Aging and gender have a strong influence on the functional capacity of the immune system. In general, the immune response in females is stronger than that in males, but there is scant information about the effect of aging on the gender difference in the immune response. To address this question, we performed a transcriptomic analysis of peripheral blood mononuclear cells derived from elderly individuals (nonagenarians, n = 146) and young controls (aged 19–30 years, n = 30). When compared to young controls, we found 339 and 248 genes that were differentially expressed (p<0.05, fold change >1.5 or <−1.5) in nonagenarian females and males, respectively, 180 of these genes were changed in both genders. An analysis of the affected signaling pathways revealed a clear gender bias: there were 48 pathways that were significantly changed in females, while only 29 were changed in males. There were 24 pathways that were shared between both genders. Our results indicate that female nonagenarians have weaker T cell defenses and a more prominent pro-inflammatory response as compared to males. In males significantly fewer pathways were affected, two of which are known to be regulated by estrogen. These data show that the effects of aging on the human immune system are significantly different in males and females.

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Section: Discussionmentioning

confidence: 99%

Transcriptional Analysis Reveals Gender-Specific Changes in the Aging of the Human Immune System

et al. 2013

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“…Female mice also have higher proportions of regulatory T cells than males, at least in response to certain viruses (33). Females exhibit higher cytotoxic T cell activity along with up-regulated expression of antiviral and proinflammatory genes, many of which have estrogen response elements in their promoters (8).…”

Section: Adaptive Immunitymentioning

confidence: 99%

Immune Cells Have Sex and So Should Journal Articles

2012

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Males and females have the same immunological cells, proteins, and pathways in place to protect against the development of disease. The kinetics, magnitude, and skewing of the responses mounted against pathogens, allergens, toxins, or self-antigens, however, can differ dramatically between the sexes. Generally, females mount higher innate and adaptive immune responses than males, which can result in faster clearance of pathogens but also contributes to increased susceptibility to inflammatory and autoimmune diseases in females compared with males. Hormonal and genetic factors contribute significantly to sex differences in immune function and disease pathogenesis. In particular, the expression of X-linked genes and microRNA as well as sex steroid hormones signaling through hormone receptors in immune cells can affect responses to immunological stimuli differently in males and females. Despite data illustrating profound differences between the sexes in immune function, sex differences in the pathogenesis of disease are often overlooked in biomedical research. Establishing journal policies that require authors to report the sex of their cells, animals, and subjects will improve our understanding of the pathogenesis of diseases, with the long-term goal of personalizing treatments for immune-mediated diseases differently for males and females in an effort to protect us equally.

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“…Thus, OGT acting through PcG would repress Oga expression and bias the cell towards sustained O-GlcNAc levels. Improper or incomplete X-inactivation is associated with a number of diseases including autoinflammatory disease [73, 74]. Subtle changes in the levels of OGT/OGA, through mechanisms just mentioned, would alter cellular O-GlcNAc levels.…”

Section: Hexosamine Signaling and Epigeneticsmentioning

confidence: 99%

O-GlcNAc cycling: Emerging roles in development and epigenetics

Love

Krause

Hanover

2010

Seminars in Cell & Developmental Biology

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The nutrient-sensing hexosamine signaling pathway modulates the levels of O-linked Nacetylglucosamine (O-GlcNAc) on key targets impacting cellular signaling, protein turnover and gene expression. O-GlcNAc cycling may be deregulated in neurodegenerative disease, cancer, and diabetes. Studies in model organisms demonstrate that the O-GlcNAc transferase (OGT/Sxc) is essential for Polycomb group (PcG) repression of the homeotic genes, clusters of genes responsible for the adult body plan. Surprisingly, from flies to man, the O-GlcNAcase (OGA, MGEA5) gene is embedded within the NK cluster, the most evolutionarily ancient of three homeobox gene clusters regulated by PcG repression. PcG repression also plays a key role in maintaining stem cell identity, recruiting the DNA methyltransferase machinery for imprinting, and in X-chromosome inactivation. Intriguingly, the Ogt gene resides near the Xist locus in vertebrates and is subject to regulation by PcG-dependent X-inactivation. OGT is also an enzymatic component of the human dosage compensation complex. These 'evo-devo' relationships linking O-GlcNAc cycling to higher order chromatin structure provide insights into how nutrient availability may influence the epigenetic regulation of gene expression. O-GlcNAc cycling at promoters and PcG repression represent concrete mechanisms by which nutritional information may be transmitted across generations in the intra-uterine environment. Thus, the nutrient-sensing hexosamine signaling pathway may be a key contributor to the metabolic deregulation resulting from prenatal exposure to famine, or the 'vicious cycle' observed in children of mothers with type-2 diabetes and metabolic disease.

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Stronger inflammatory/cytotoxic T cell response in women identified by microarray analysis

Cited by 28 publications

References 2 publications

Transcriptional Analysis Reveals Gender-Specific Changes in the Aging of the Human Immune System

Transcriptional Analysis Reveals Gender-Specific Changes in the Aging of the Human Immune System

Immune Cells Have Sex and So Should Journal Articles

O-GlcNAc cycling: Emerging roles in development and epigenetics

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