Literature DB >> 27890000

Reproductive Toxicity of T Cells in Early Life: Abnormal Immune Development and Postnatal Diseases.

Han-Xiao Liu1, Aifang Jiang2, Ting Chen1, Wen Qu1, Hui-Yi Yan1, Jie Ping3.   

Abstract

Immunity is a balanced status with adequate biological defenses to recognize and fight "non-self", as well as adequate tolerance to recognize "self". To maintain this immune homeostasis, a well-organized T cell immune network is required, which in part depends on the well-controlled development of alternative effector T cells, with different cytokine repertoires. Recent researches have pointed that developing fetal T cells network is a remarkably sensitive toxicological target for adverse factors in early life. Epidemiological and experimental studies showed an inseparable relationship between T cell developmental toxicity and immune diseases in adults. Considering that the inflammatory and immune disorders have become a growing health problem worldwide, increasing attention is now being paid to the T cell developmental toxicity. We propose that adverse factors may have programming effects on the crucial functions of immune system during early life which is critical for fetal T cell development and the establishment of the distinct T cell repertoires balance. The permanently disturbed intrathymic or peripheral T cell development may in turn lead to the immune disorders in later life. In this manuscript, we reviewed how adverse factors affected T cell development in early-life with the consequence of the immune dysfunction and immune diseases, and further elucidate the mechanisms. These mechanisms will be helpful in prevention and treatment of the increased prevalence of immune diseases by interfering those pathways. Copyright© Bentham Science Publishers; For any queries, please email at epub@benthamscience.org.

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Keywords:  Immunotoxicology; T cells; immune diseases; reproductive toxicity; thymocytes; thymus

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Year:  2017        PMID: 27890000     DOI: 10.2174/1389450117666161124145641

Source DB:  PubMed          Journal:  Curr Drug Targets        ISSN: 1389-4501            Impact factor:   3.465


  1 in total

1.  α7 nAChR mediated Fas demethylation contributes to prenatal nicotine exposure-induced programmed thymocyte apoptosis in mice.

Authors:  Han-Xiao Liu; Sha Liu; Wen Qu; Hui-Yi Yan; Xiao Wen; Ting Chen; Li-Fang Hou; Jie Ping
Journal:  Oncotarget       Date:  2017-10-05
  1 in total

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