Human Prolactin Promotes Human Secondary Immunoglobulin Response in Human/SCID Mouse Chimeras

Zhang, Jian; Sun, Rui; Tian, Zhigang

doi:10.1128/cvi.00244-06

Cited by 8 publications

(5 citation statements)

References 32 publications

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“…Previous studies also showed that peripheral blood B cells secrete higher levels of antibodies following treatment with human prolactin and IL-2 in vitro, in a dose-dependent manner [25,28]. Also, a study of human/SCID mouse showed that human recombinant prolactin can promote increased IgG production in a secondary response [29]. This is not in accordance with our study, as we found no correlation between prolactin and total immunoglobulin levels.…”

Section: Discussioncontrasting

confidence: 78%

Immunomodulating Effects Depend on Prolactin Levels in Patients with Hyperprolactinemia

et al. 2020

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Prolactin is known to have immune modulatory effects acting through the prolactin receptor, which is present on a variety of immune cells. Certain chemokines contribute to form the type of T helper (Th) preponderance in the immune response. The objective of this work was to assess if hyperprolactinemia not related to pregnancy is associated with changes in circulating levels of chemokines and other immunological markers. In this cross sectional study, 35 patients with hyperprolactinemia (5 men), and 102 healthy blood donors (19 men) were included. Serum levels of Th1- Th2- and Th17-associated chemokines, C-reactive protein, immunoglobulins, and the B cell attracting chemokine CXCL13 were assessed. The hyperprolactinemic group had significantly higher levels of Th2 associated CCL22 (p=0.022), Th17 associated CXCL1 (p=0.001), B cell attracting CXCL13 (p=0.003), and C-reactive protein (p<0.001) compared to controls, and these proteins were also positively correlated with prolactin levels. While differences in CCL22, CXCL1, CXCL13, and C-reactive protein were present in patients with low or moderate hyperprolactinemia, no differences were observed at high (>3600 mU/l) prolactin levels. To evaluate a possible dose-associated response to prolactin, an in vitro model was used, showing prolactin-induced increase in T-helper cell activation at moderate levels, while activation decreased at higher levels. Hyperprolactinemia seems to have several immunomodulatory effects and was associated with increased levels of chemokines associated with Th2 and Th17 responses and B cell attraction. However, patients with greatly increased prolactin had normal levels of chemokines, and in vitro, high levels of prolactin decreased T-helper cell activation.

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Section: Discussioncontrasting

confidence: 78%

Immunomodulating Effects Depend on Prolactin Levels in Patients with Hyperprolactinemia

et al. 2020

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“…Although REM sleep might also support adaptive immune functions, the pro-inflammatory endocrine milieu present during SWS (including high levels of GH, prolactin, and aldosterone and nadir levels of cortisol) is optimally suited for promoting APC-T cell interactions. GH, prolactin, and aldosterone are known to support T-cell migration, the release of pro-inflammatory and Th1 cytokines, cell proliferation, and lymphocyte responses to a microbial challenge (43, 45, 48, 117, 126, 286, 355, 362–365, 380, 389, 478, 516, 518, 524, 575, 583, 601). On the other hand, low levels of cortisol during SWS could allow efficient APC-T cell interactions (157, 211, 417, 427, 438).…”

Section: Sleep Effects On Host Defensementioning

confidence: 99%

The Sleep-Immune Crosstalk in Health and Disease

Besedovsky

Lange

Haack

2019

Physiological Reviews

952

759

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Sleep and immunity are bidirectionally linked. Immune system activation alters sleep, and sleep in turn affects the innate and adaptive arm of our body’s defense system. Stimulation of the immune system by microbial challenges triggers an inflammatory response, which, depending on its magnitude and time course, can induce an increase in sleep duration and intensity, but also a disruption of sleep. Enhancement of sleep during an infection is assumed to feedback to the immune system to promote host defense. Indeed, sleep affects various immune parameters, is associated with a reduced infection risk, and can improve infection outcome and vaccination responses. The induction of a hormonal constellation that supports immune functions is one likely mechanism underlying the immune-supporting effects of sleep. In the absence of an infectious challenge, sleep appears to promote inflammatory homeostasis through effects on several inflammatory mediators, such as cytokines. This notion is supported by findings that prolonged sleep deficiency (e.g., short sleep duration, sleep disturbance) can lead to chronic, systemic low-grade inflammation and is associated with various diseases that have an inflammatory component, like diabetes, atherosclerosis, and neurodegeneration. Here, we review available data on this regulatory sleep-immune crosstalk, point out methodological challenges, and suggest questions open for future research.

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“…IgG is an immunoglobulin secreted by plasmocyte when mature B cells are differentiated into plasmocytes by antigen stimulation. It is reported that human-derived IgG can be used to assess whether immune function of SCID mouse with hu-PBL engraftment is reconstructed [ 17 , 18 ] and that antigen stimulation promotes human secondary IgG responses in hu-PBL/SCID mouse [ 19 , 20 ]. Interestingly, a significantly positive relationship exists between the appearance of human IgG and tumorigenesis of B-cell lymphoma in the findings of our present study.…”

Section: Discussionmentioning

confidence: 99%

Human-derived IgG level as an indicator for EBV-associated lymphoma model in Hu-PBL/SCID chimeras

Tang

Zhang

et al. 2011

Virol J

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BackgroundEpstein-Barr virus (EBV) has a close association with various types of human lymphomas. Animal models are essential to elucidate the pathogenesis of human EBV-associated lymphomas. The aim of the present study is to evaluate the association between human IgG concentration and EBV-associated lymphoma development in huPBL/SCID mice.MethodsHuman peripheral blood lymphocytes (hu-PBL) from EBV-seropositive donors were inoculated intraperitoneally into SCID mouse. Immunohistochemical staining was used to examine differentiated antigens of tumor cells. EBV infection of the induced tumors was detected by in situ hybridization. IgG concentrations in the serums of 12 SCID mice were measured by unidirectional immunodiffusion assay.Results21 out of 29 mice developed tumors in their body. Immunohistochemical staining showed that all induced tumors were LCA (leukocyte common antigen) positive, B-cell markers (CD20, CD79a) positive, and T-cell markers (both CD3 and CD45RO) negative. The tumors can be diagnosed as human B-cell lymphomas by these morphological and immunohistochemical features. In situ hybridization exhibited resultant tumor cells had EBV encoded small RNA-1 (EBER-1). Human-derived IgG could be found in the serum from SCID mice on the 15th day following hu-PBL transplantation, and IgG levels increased with the tumor development in 6 hu-PBL/SCID chimeras.ConclusionsIntraperitoneal transfer of hu-PBLs from EBV+ donors to SCID mice leads to high human IgG levels in mouse serum and B cell lymphomas. Our findings suggest that increasing levels of human-derived IgG in peripheral blood from hu-PBL/SCID mice could be used to monitor EBV-related human B-cell lymphoma development in experimental animals.

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Human Prolactin Promotes Human Secondary Immunoglobulin Response in Human/SCID Mouse Chimeras

Abstract: Recombinant human prolactin (rhPRL) was administered to huPBL-SCID mice to determine its effects on production of human immunoglobulin (

Cited by 8 publications

References 32 publications

Immunomodulating Effects Depend on Prolactin Levels in Patients with Hyperprolactinemia

Immunomodulating Effects Depend on Prolactin Levels in Patients with Hyperprolactinemia

The Sleep-Immune Crosstalk in Health and Disease

Human-derived IgG level as an indicator for EBV-associated lymphoma model in Hu-PBL/SCID chimeras

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