Autoimmune disease and gender: Plausible mechanisms for the female predominance of autoimmunity

A large number of autoimmune diseases (ADs) are more prevalent in women. The more frequent the AD and the later it appears, the more women are affected. Many ideas mainly based on hormonal and genetic factors that influence the autoimmune systems of females and males differently, have been proposed...

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Tipo de recurso:
Fecha de publicación:
2012
Institución:
Universidad del Rosario
Repositorio:
Repositorio EdocUR - U. Rosario
Idioma:
eng
OAI Identifier:
oai:repository.urosario.edu.co:10336/22252
Acceso en línea:
https://doi.org/10.1016/j.jaut.2011.10.003
https://repository.urosario.edu.co/handle/10336/22252
Palabra clave:
Androgen
Bromocriptine
Estrogen
Estrogen receptor
Prolactin
Antibody production
Article
Autoimmune disease
Autoimmunity
B lymphocyte activation
Cd4 lymphocyte count
Cd8+ t lymphocyte
Cellular immunity
Disease association
Disease predisposition
Genetic risk
Hormonal regulation
Human
Humoral immunity
Klinefelter syndrome
Lymphoma
Microchimerism
Monocyte
Monosomy x
Multiple sclerosis
Natural killer cell
Neutrophil
Onset age
Pregnancy
Pregnancy outcome
Prevalence
Priority journal
Raynaud phenomenon
Receptor binding
Rheumatoid arthritis
Sex difference
Sjoegren syndrome
Systemic lupus erythematosus
Systemic sclerosis
T lymphocyte activation
Th1 cell
Th2 cell
X chromosome
X chromosome inactivation
Y chromosome
Autoimmune diseases
Autoimmunity
Chimerism
Female
Hormones
Humans
Male
Pregnancy
Sex factors
Autoimmune diseases
Gender differences
Sex hormones
X chromosome
human
x
Chromosomes
Rights
License
Abierto (Texto Completo)
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dc.title.spa.fl_str_mv Autoimmune disease and gender: Plausible mechanisms for the female predominance of autoimmunity
title Autoimmune disease and gender: Plausible mechanisms for the female predominance of autoimmunity
spellingShingle Autoimmune disease and gender: Plausible mechanisms for the female predominance of autoimmunity
Androgen
Bromocriptine
Estrogen
Estrogen receptor
Prolactin
Antibody production
Article
Autoimmune disease
Autoimmunity
B lymphocyte activation
Cd4 lymphocyte count
Cd8+ t lymphocyte
Cellular immunity
Disease association
Disease predisposition
Genetic risk
Hormonal regulation
Human
Humoral immunity
Klinefelter syndrome
Lymphoma
Microchimerism
Monocyte
Monosomy x
Multiple sclerosis
Natural killer cell
Neutrophil
Onset age
Pregnancy
Pregnancy outcome
Prevalence
Priority journal
Raynaud phenomenon
Receptor binding
Rheumatoid arthritis
Sex difference
Sjoegren syndrome
Systemic lupus erythematosus
Systemic sclerosis
T lymphocyte activation
Th1 cell
Th2 cell
X chromosome
X chromosome inactivation
Y chromosome
Autoimmune diseases
Autoimmunity
Chimerism
Female
Hormones
Humans
Male
Pregnancy
Sex factors
Autoimmune diseases
Gender differences
Sex hormones
X chromosome
human
x
Chromosomes
title_short Autoimmune disease and gender: Plausible mechanisms for the female predominance of autoimmunity
title_full Autoimmune disease and gender: Plausible mechanisms for the female predominance of autoimmunity
title_fullStr Autoimmune disease and gender: Plausible mechanisms for the female predominance of autoimmunity
title_full_unstemmed Autoimmune disease and gender: Plausible mechanisms for the female predominance of autoimmunity
title_sort Autoimmune disease and gender: Plausible mechanisms for the female predominance of autoimmunity
dc.subject.keyword.spa.fl_str_mv Androgen
Bromocriptine
Estrogen
Estrogen receptor
Prolactin
Antibody production
Article
Autoimmune disease
Autoimmunity
B lymphocyte activation
Cd4 lymphocyte count
Cd8+ t lymphocyte
Cellular immunity
Disease association
Disease predisposition
Genetic risk
Hormonal regulation
Human
Humoral immunity
Klinefelter syndrome
Lymphoma
Microchimerism
Monocyte
Monosomy x
Multiple sclerosis
Natural killer cell
Neutrophil
Onset age
Pregnancy
Pregnancy outcome
Prevalence
Priority journal
Raynaud phenomenon
Receptor binding
Rheumatoid arthritis
Sex difference
Sjoegren syndrome
Systemic lupus erythematosus
Systemic sclerosis
T lymphocyte activation
Th1 cell
Th2 cell
X chromosome
X chromosome inactivation
Y chromosome
Autoimmune diseases
Autoimmunity
Chimerism
Female
Hormones
Humans
Male
Pregnancy
Sex factors
Autoimmune diseases
Gender differences
Sex hormones
X chromosome
topic Androgen
Bromocriptine
Estrogen
Estrogen receptor
Prolactin
Antibody production
Article
Autoimmune disease
Autoimmunity
B lymphocyte activation
Cd4 lymphocyte count
Cd8+ t lymphocyte
Cellular immunity
Disease association
Disease predisposition
Genetic risk
Hormonal regulation
Human
Humoral immunity
Klinefelter syndrome
Lymphoma
Microchimerism
Monocyte
Monosomy x
Multiple sclerosis
Natural killer cell
Neutrophil
Onset age
Pregnancy
Pregnancy outcome
Prevalence
Priority journal
Raynaud phenomenon
Receptor binding
Rheumatoid arthritis
Sex difference
Sjoegren syndrome
Systemic lupus erythematosus
Systemic sclerosis
T lymphocyte activation
Th1 cell
Th2 cell
X chromosome
X chromosome inactivation
Y chromosome
Autoimmune diseases
Autoimmunity
Chimerism
Female
Hormones
Humans
Male
Pregnancy
Sex factors
Autoimmune diseases
Gender differences
Sex hormones
X chromosome
human
x
Chromosomes
dc.subject.keyword.eng.fl_str_mv human
x
Chromosomes
description A large number of autoimmune diseases (ADs) are more prevalent in women. The more frequent the AD and the later it appears, the more women are affected. Many ideas mainly based on hormonal and genetic factors that influence the autoimmune systems of females and males differently, have been proposed to explain this predominance. These hypotheses have gained credence mostly because many of these diseases appear or fluctuate when there are hormonal changes such as in late adolescence and pregnancy. Differences in X chromosome characteristics between men and women with an AD have led researchers to think that the genetic background of this group of diseases also relates to the genetic determinants of gender. These hormonal changes as well as the genetic factors that could explain why women are more prone to develop ADs are herein reviewed. © 2011 Elsevier Ltd.
publishDate 2012
dc.date.created.spa.fl_str_mv 2012
dc.date.accessioned.none.fl_str_mv 2020-05-25T23:55:53Z
dc.date.available.none.fl_str_mv 2020-05-25T23:55:53Z
dc.type.eng.fl_str_mv article
dc.type.coarversion.fl_str_mv http://purl.org/coar/version/c_970fb48d4fbd8a85
dc.type.coar.fl_str_mv http://purl.org/coar/resource_type/c_6501
dc.type.spa.spa.fl_str_mv Artículo
dc.identifier.doi.none.fl_str_mv https://doi.org/10.1016/j.jaut.2011.10.003
dc.identifier.issn.none.fl_str_mv 10959157
08968411
dc.identifier.uri.none.fl_str_mv https://repository.urosario.edu.co/handle/10336/22252
url https://doi.org/10.1016/j.jaut.2011.10.003
https://repository.urosario.edu.co/handle/10336/22252
identifier_str_mv 10959157
08968411
dc.language.iso.spa.fl_str_mv eng
language eng
dc.relation.citationEndPage.none.fl_str_mv J119
dc.relation.citationIssue.none.fl_str_mv No. 43892
dc.relation.citationStartPage.none.fl_str_mv J109
dc.relation.citationTitle.none.fl_str_mv Journal of Autoimmunity
dc.relation.citationVolume.none.fl_str_mv Vol. 38
dc.relation.ispartof.spa.fl_str_mv Journal of Autoimmunity, ISSN:10959157, 08968411, Vol.38, No.43892 (2012); pp. J109-J119
dc.relation.uri.spa.fl_str_mv https://www.scopus.com/inward/record.uri?eid=2-s2.0-84858752604&doi=10.1016%2fj.jaut.2011.10.003&partnerID=40&md5=4fc01085acc4c00466ee71ba1c29724d
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