Sex Hormones and the Genesis of Autoimmunity

Ackerman, Lindsay

doi:10.1001/archderm.142.3.371

Cited by 102 publications

(158 citation statements)

References 47 publications

(132 reference statements)

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“…7,8 A consistent clinical observation is that women develop autoimmune diseases much more frequently than men. 7,9,10 Furthermore, epidemiologic studies have demonstrated that a history of autoimmune diseases is a significant risk for the subsequent development of lymphoma and multiple myeloma. [11][12][13] The sexually distinct patterns of autoimmune diseases have been, at least in part, attributed to sex hormones, particularly estrogens.…”

mentioning

confidence: 90%

“…Estrogens are important immunomodulators, exerting significant effects on cell proliferation, apoptosis, cytokine production and differentiation of hematopoietic cells. [5][6][7] Estrogen receptors (both alpha and beta) are expressed on normal B and T lymphocytes, bone marrow, and in leukemia and lymphoma cell lines. 7,8 A consistent clinical observation is that women develop autoimmune diseases much more frequently than men.…”

mentioning

confidence: 99%

“…[5][6][7] Estrogen receptors (both alpha and beta) are expressed on normal B and T lymphocytes, bone marrow, and in leukemia and lymphoma cell lines. 7,8 A consistent clinical observation is that women develop autoimmune diseases much more frequently than men. 7,9,10 Furthermore, epidemiologic studies have demonstrated that a history of autoimmune diseases is a significant risk for the subsequent development of lymphoma and multiple myeloma.…”

mentioning

confidence: 99%

“…[11][12][13] The sexually distinct patterns of autoimmune diseases have been, at least in part, attributed to sex hormones, particularly estrogens. 5,7,10 Estrogens induce activation-induced deaminase, leading to somatic hypermutation and production of autoantibodies. 5 However, progesterone exert opposite effects to estrogens in vitro, particularly at lower physiological levels, whereas the vivo effect of progesterone seems to be more complex, depending on hormone concentrations and other gonadal factors.…”

mentioning

confidence: 99%

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Menopausal estrogen therapy and non‐Hodgkin's lymphoma: A post‐hoc analysis of women's health initiative randomized clinical trial

Kato

Chlebowski

Hou

et al. 2015

Intl Journal of Cancer

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Estrogens are important immunomodulators, exerting significant effects on cell proliferation, apoptosis, cytokine production and differentiation of hematopoietic cells. Estrogen receptors are expressed on normal B and T lymphocytes, bone marrow and in leukemia and lymphoma cell lines. Epidemiologic evidence for the association of menopausal hormone use with risk of non-Hodgkin's lymphoma (NHL) has been mixed; however, all of the investigations have been observational. We analyzed the data from Women's Health Initiative hormone therapy trials where conjugated equine estrogens (CEE; 0.625 mg/d) plus medroxyprogesterone acetate (MPA; 2.5 mg/d) (n 5 16,654) or CEE alone (women with prior hysterectomy) (n 5 10,685) were tested against placebos and the intervention lasted a median of 5.6 years in the CEE 1 MPA trial and 7.2 years in the CEE alone trial. During 13 years of follow-up through September 20, 2013 383 incident NHL cases were identified. We used the intent-to-treat approach to calculate incidence rates of NHL, hazards ratios (HR) and 95% confidence intervals (CI) by treatment group. Incidence of NHL was virtually the same in the treatment and placebo groups. The HR was 1.02 (95%CI 0.74-1.39) for CEE alone, 0.98 (95% CI 0.76-1.28) for CEE1MPA, and 1.00 (95% CI 0.82-1.22) for both combined. There were no specific NHL subtypes associated with either type of the treatment, except a marginally decreased risk of plasma cell neoplasms (HR5 0.53 95% CI 0.27-1.03) in the CEE-alone group. These results do not support a role of estrogen alone or combined with progestin in the development of NHL among postmenopausal women.Lymphoid neoplasms, including lymphoma, myeloma and lymphocytic leukemia, comprise the 5th most commonly diagnosed cancer in the United States, 1 following breast, prostate, lung and colorectal cancers. Although lymphoid neoplasms are clinically and etiologically heterogeneous, to a large extent, severe disruption of immune function has been

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confidence: 90%

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confidence: 99%

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confidence: 99%

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confidence: 99%

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Menopausal estrogen therapy and non‐Hodgkin's lymphoma: A post‐hoc analysis of women's health initiative randomized clinical trial

Kato

Chlebowski

Hou

et al. 2015

Intl Journal of Cancer

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“…Adult rats were immunized at the base of the tail with 75 mg of the peptide MBP [68][69][70][71][72][73][74][75][76][77][78][79][80][81][82][83][84][85][86] (YGSLPQKSQR-SQDENPV) 27 (synthesized at the Weizmann Institute of Science), emulsified in an equal volume of complete Freund's adjuvant (CFA; DIFCO LABORA-TORIES, Detroit, MI, USA) containing 5 mg ml…”

Section: Vaccinationmentioning

confidence: 99%

Dysregulation of kisspeptin and neurogenesis at adolescence link inborn immune deficits to the late onset of abnormal sensorimotor gating in congenital psychological disorders

et al. 2009

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Neuropsychological syndromes including schizophrenia often do not manifest until late adolescence or early adulthood. Studies attributing a role in brain maintenance to the immune system led us to propose that malfunction of immune-dependent regulation of brain functions at adolescence underlies the late onset of such diseases/syndromes. One such function is sensorimotor gating, the ability to segregate a continuous stream of sensory and cognitive information, and to selectively allocate attention to a significant event by silencing the background (measured by prepulse inhibition; PPI). This activity is impaired in schizophrenia, as well as in several other neuropsychological diseases. Using a model of prenatal immune activation (maternal polyriboinosinic-polyribocytidylic acid (poly I:C) injection), often used as a model for schizophrenia, and in which abnormal PPI has a delayed appearance, we demonstrated a form of immune deficit in the adult offspring. Similar abnormal PPI with a delayed appearance was found in congenitally immune-deficient mice (severe combined immune deficient, SCID), and could be reversed by immune reconstitution. This functional deficit correlated with impairment of both hippocampal neurogenesis and expression of the gene encoding kisspeptin (Kiss1) that manifested at adulthood. Moreover, exogenous administration of a kisspeptin-derived peptide partially reversed the gating deficits in the SCID mice. Our results suggest that a form of congenital immune deficiency may be a key factor that determines manifestation of developmental neuropsychological disorders with onset only at early adulthood.

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Women's Dermatologic Diseases, Health Care Delivery, and Socioeconomic Barriers

Robinson¹,

Ramos-e-Siliva²

2006

Arch Dermatol

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Sex Hormones and the Genesis of Autoimmunity

Cited by 102 publications

References 47 publications

Menopausal estrogen therapy and non‐Hodgkin's lymphoma: A post‐hoc analysis of women's health initiative randomized clinical trial

Menopausal estrogen therapy and non‐Hodgkin's lymphoma: A post‐hoc analysis of women's health initiative randomized clinical trial

Dysregulation of kisspeptin and neurogenesis at adolescence link inborn immune deficits to the late onset of abnormal sensorimotor gating in congenital psychological disorders

Women's Dermatologic Diseases, Health Care Delivery, and Socioeconomic Barriers

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