scholarly journals Discordance of Twin Placentas for Multifocal Eosinophilic/T-cell Chorionic Vasculitis

2018 ◽  
Vol 22 (1) ◽  
pp. 40-44
Author(s):  
Erik W Nohr ◽  
James R Wright
Keyword(s):  
Immune System ◽  
T Cell ◽  
T Lymphocytes ◽  
Monozygotic Twin ◽  
Vascular Territory ◽  
Twin Pregnancies ◽  
Fetal Immune System

Eosinophilic/T-cell chorionic vasculitis (ETCV) is an idiopathic placental lesion characterized by chorionic vasculitis composed predominantly of eosinophils and CD3+ T lymphocytes. It usually presents as a unifocal lesion, but a subset have multifocal involvement. We report 4 Di-Di and 2 Di-Mo twins sharing fused placental discs with discordant circulatory involvement by multifocal ETCV. The findings are difficult to explain by sampling alone. The limitation of ETCV to 1 fetus’s vascular territory in monozygotic twin pregnancies is difficult to explain but could provide insights into the fetal immune system and the etiology of ETCV.

Lenalidomide IS Able to Restore Immune SYSTEM IN MULTIPLE MYELOMA PATIENTS.

Blood ◽  
2009 ◽  
Vol 114 (22) ◽  
pp. 4909-4909 ◽  
Author(s):  
Annalisa Chiarenza ◽  
Nunziatina Parrinello ◽  
Piera La Cava ◽  
Eleonora Spina ◽  
Daniele Tibullo ◽  
...  
Keyword(s):  
Multiple Myeloma ◽  
Immune System ◽  
T Cell ◽  
T Lymphocytes ◽  
Mononuclear Cells ◽  
Conflicts Of Interest ◽  
Gradient Centrifugation ◽  
Target Cells ◽  
First Line ◽  
Number Of Patients

Abstract Abstract 4909 LENALIDOMIDE IS ABLE TO RESTORE IMMUNE SYSTEM IN MULTIPLE MYELOMA PATIENTS Annalisa Chiarenza, Nunziatina Parrinello, Piera La Cava, Eleonora Spina, Daniele Tibullo, Cesarina Giallongo, Maide Cavalli, Alessandra Romano, Paolo Fiumara, Giuseppe A. Palumbo, Francesco Di Raimondo Background Multiple myeloma (MM) is a malignant plasma-cell proliferative disorder associated with dysfunctional T-cell responses. The immunomodulatory Thal derivative (IMiD) CC-5013 (lenalidomide) appears to be a promising agent for the treatment of myeloma. Although the exact antitumor mechanism of action of lenalidomide is unknown, a number of mechanisms are postulated to be responsible for it's activity (inhibition of angiogenesis, direct antiproliferative and proapoptotic effects on MM cells, suppression of pro-inflammatory cytokines, modulation of myeloma-stromal cells adhesive interactions). In addition, it has been demonstrated that lenalidomide in vitro is able to enhance T cell proliferation and to promotes ADCC. In this study we evaluated if MM patients have a deficit of T-reg (CD4+, CD25+, and FOXP3+) and of T lymphocytes bearing CD200 (a tolerogenic molecule) and the effect of lenalidomide treatment on these parameters. In addition, we investigated whether lenalidomide could improve ex vivo the ADCC against myeloma cells. Materials and methods Eight patients with previously untreated MM (median age 56 years) were treated with lenalidomide plus dexamethasone as first line therapy. Lenalidomide was given orally 25 mg daily on days 1 to 21 of a 28-day cycle. Dexamethasone was given orally 40 mg daily on days 1, 8, 15, 22 of each cycle. All patients were evaluable for response and toxicity. Peripheral blood mononuclear cells (PBMNc) were obtained from MM patients using density gradient centrifugation (Fycoll) under sterile condictions, at the beginning of treatment and after 4 cycles of therapy. The percentage of T-reg (CD4+CD25+FOXP3+) and the expression of CD200 on T- lymphocytes were evaluated by cytometry. Twelve healthy subjects were used as control. Moreover, PBMNc (effector cells, E) were incubated with MM cells line ARH-77 (target cells, T), previously labelled with CFDA,SE (carboxyfluorescein diacetate, succinimidyl ester) as a tracing fluorescent marker, in culture medium (RPMI-1640, 10%FCS, 1%penicillin/streptomycin) at different concentration (T/E ratio 1:20, 1:40). After 18-24 h co-colture cells were analyzed by flow cytometry and MM plasma cells cytotoxicity was calculated as the percentage of positive CFDA,SE/propidium cells. Myeloma cell viability was determined by tripan blue esclusion and apoptosis was also evaluated using Annexin V/propidium assay. Two MM patients treated in first line with a combination of Velcade, Thalidomide and Dexamethasone (VTD) were used as control and the experiments were performed in duplicate. Results MM patients have a significantly lower rate of CD4+/CD25+/FOXP3+ and CD200+/CD3+ than normal (28,3±14,9/mmc and 37,8±24,7 /mmc vs 79,3±27,8 and 79,5± 48,9)(p=0,0001 and p=0,01 respectively). In our study, lenalidomide treatment resulted in an increase both of Treg cells and T-lymphocytes espressing CD200. This improvement is not statistically significant probably due to the low number of patients examined (tab I). More important, we observed that PBMC derived from patients treated with lenalidomide showed an increase ability to kill a target MM cell line compared to PBMC collected at diagnosis (CFDA,SE/propidium cells 11% vs 68%). This effect was more prominent in patients treated with lenalidomide than in MM patients treated with VTD (CFDA,SE/propidium cells 12% vs 39%), Fig.1. Conclusions Our data emphasize the role of lenalidomide in modulating the endogenous tumor-specific immune response and underline the anti-myeloma activity of these new class of drugs. Disclosures No relevant conflicts of interest to declare.

scholarly journals ROLE OF DISTINCT CD4+ T-CELL SUBSETS IN HIV-INFECTION PATHOGENESIS

2020 ◽  
pp. 236-246
Author(s):  
E. V. Saidakova ◽  
Keyword(s):  
Immune System ◽  
T Cell ◽  
T Lymphocytes ◽  
Hiv Infection ◽  
T Lymphocyte ◽  
Highly Active Antiretroviral Therapy ◽  
T Cell Subsets ◽  
Cd4 T Cell ◽  
Effector Memory ◽  
T Lymphocyte Subsets

CD4+ T-cell pool is composed of cells residing in different maturation stages. Naive CD4+ T-lymphocytes, CD4+ stem memory T-cells, CD4+ central and effector memory T-lymphocytes perform var-ious functions in maintaining the immune system homeostasis. Despite phenotypic differences, each of those cells can be infected with HIV. Specific features of distinct CD4+ T-lymphocyte subsets determine their role in HIV-infection pathogenesis. By analyzing changes of CD4+ T-lymphocyte subset composi-tion, one can estimate the degree of the immune system damage and make predictions of immune recov-ery under highly active antiretroviral therapy. The article summarizes the main events occurring with CD4+ T-cell subsets during HIV-infection.

scholarly journals Intrauterine Transfusions Affect Fetal T-Cell Immunity

Blood ◽  
1997 ◽  
Vol 90 (6) ◽  
pp. 2492-2501 ◽  
Author(s):  
Henk E. Viëtor ◽  
Gail E. Hawes ◽  
Claudia van den Oever ◽  
Els van Beelen ◽  
Humphrey H.H. Kanhai ◽  
...  
Keyword(s):  
Immune System ◽  
T Cell ◽  
Cell Receptor ◽  
Hemolytic Disease ◽  
Cell Immunity ◽  
Intrauterine Transfusion ◽  
Qualitative Nature ◽  
The Individual ◽  
Complementarity Determining Region ◽  
Fetal Immune System

Abstract Intrauterine transfusion (IUT) therapy is the treatment of choice in severe hemolytic disease of the fetus. This treatment automatically implies the introduction of alloantigens in the fetal circulation, which might potentially influence the unprimed fetal immune system. The present study provides evidence that the fetal immune system is indeed prone to modulations of the T-cell receptor BV (TCRBV) repertoire as a result of IUT treatment. Most notably, IUT therapy affects the composition of the CD4+ repertoire, whereas this effect may be obscured in the CD8+ subset. The CD8+ subset was found to be influenced by alterations of the TCRBV repertoire both in IUT patients and controls, suggesting that modulations in this subset could be the result of developmental influences. A more detailed analysis on the composition of the individual TCRBV families was performed by evaluating the distribution of the complementarity determining region 3 (CDR3) size lengths of [32P]-radiolabeled TCRBV transcripts. Using this technique, referred to as spectratyping, only marginal changes were observed in the CD4+ and CD8+ subset during the course of treatment and gestational development of both IUT-treated patients and controls. Therefore, the alterations in the overall TCRBV repertoire were of a quantitative rather than a qualitative nature. To evaluate whether the observed alterations in TCRBV usage-frequencies were a reflection of an allo-reactive response, a primed lymphocyte test (PLT) was performed in 3 IUT-treated patients. We observed that IUT, performed as early as 23 weeks of gestation, may induce the establishment of memory T cells against the IUT donor. However, there was no association between the observed changes in TCRBV repertoire and the magnitude of the secondary allo-reactive response.

scholarly journals Intrauterine Transfusions Affect Fetal T-Cell Immunity

Blood ◽  
1997 ◽  
Vol 90 (6) ◽  
pp. 2492-2501
Author(s):  
Henk E. Viëtor ◽  
Gail E. Hawes ◽  
Claudia van den Oever ◽  
Els van Beelen ◽  
Humphrey H.H. Kanhai ◽  
...  
Keyword(s):  
Immune System ◽  
T Cell ◽  
Cell Receptor ◽  
Hemolytic Disease ◽  
Cell Immunity ◽  
Intrauterine Transfusion ◽  
Qualitative Nature ◽  
The Individual ◽  
Complementarity Determining Region ◽  
Fetal Immune System

Intrauterine transfusion (IUT) therapy is the treatment of choice in severe hemolytic disease of the fetus. This treatment automatically implies the introduction of alloantigens in the fetal circulation, which might potentially influence the unprimed fetal immune system. The present study provides evidence that the fetal immune system is indeed prone to modulations of the T-cell receptor BV (TCRBV) repertoire as a result of IUT treatment. Most notably, IUT therapy affects the composition of the CD4+ repertoire, whereas this effect may be obscured in the CD8+ subset. The CD8+ subset was found to be influenced by alterations of the TCRBV repertoire both in IUT patients and controls, suggesting that modulations in this subset could be the result of developmental influences. A more detailed analysis on the composition of the individual TCRBV families was performed by evaluating the distribution of the complementarity determining region 3 (CDR3) size lengths of [32P]-radiolabeled TCRBV transcripts. Using this technique, referred to as spectratyping, only marginal changes were observed in the CD4+ and CD8+ subset during the course of treatment and gestational development of both IUT-treated patients and controls. Therefore, the alterations in the overall TCRBV repertoire were of a quantitative rather than a qualitative nature. To evaluate whether the observed alterations in TCRBV usage-frequencies were a reflection of an allo-reactive response, a primed lymphocyte test (PLT) was performed in 3 IUT-treated patients. We observed that IUT, performed as early as 23 weeks of gestation, may induce the establishment of memory T cells against the IUT donor. However, there was no association between the observed changes in TCRBV repertoire and the magnitude of the secondary allo-reactive response.

Prolactin receptor expression in lymphocytes from patients with hyperprolactinemia or acromegaly

1995 ◽  
Vol 147 (2) ◽  
pp. 353-359 ◽  
Author(s):  
M C Leite-de-Moraes ◽  
P Touraine ◽  
P A Kelly ◽  
F Kuttenn ◽  
M Dardenne
Keyword(s):  
Immune System ◽  
T Cell ◽  
T Lymphocytes ◽  
B Lymphocytes ◽  
Peripheral Blood ◽  
Blood Cells ◽  
Matched Control ◽  
Prolactin Receptor ◽  
Receptor Expression ◽  
Prolactin Receptors

Abstract Previous reports demonstrated that prolactin receptors (PRL-R) are widely expressed on cells of the immune system. We analyzed a possible regulation of PRL-R expression on human mononucleated blood cells by prolactin (PRL) itself. PRL-R expression was analyzed by immunofluorescence on T and B lymphocytes and monocytes from peripheral blood mononucleated cells (PBMC) of patients with hyperprolactinemia or acromegaly compared with sex- and age-matched control subjects. The frequency of PRL-R positive cells and the intensity of PRL-R expression was only modified among the CD8+ T cell population of hyperprolactinemic patients with macroadenoma. No correlation was reported between PRL-R expression and circulating PRL levels. The percentage of PRL-R+ cells on B or T lymphocytes and monocytes as well as the capacity of PBMC to proliferate in response to T cell mitogens were not significantly different in bromocriptine-treated compared with untreated patients. These findings suggest that factors other than pituitary PRL play the major role in regulating PRL-R expression on cells of the immune system. Journal of Endocrinology (1995) 147, 353–359

Peculiarities of the immune status of patients with multidrug­resistant pulmonary tuberculosis after application of treatment regimens with bedaquiline and linezolid

2021 ◽  
pp. 30-35
Author(s):  
N.Ye. Lapovets ◽  
O.A. Tkach ◽  
I.L. Platonova ◽  
L.Ye. Lapovets ◽  
V.M. Akimova
Keyword(s):  
Immune System ◽  
T Cell ◽  
T Lymphocytes ◽  
Pulmonary Tuberculosis ◽  
Differential Count ◽  
Hypersensitivity Reactions ◽  
Treatment Regimens ◽  
Fourth Type ◽  
T Cell Immunodeficiency ◽  
T Helpers

Objective — to investigate immuno-metabolic homeostasis in patients with new and recurrent cases of destructive forms of multidrug-resistant pulmonary tuberculosis (MDR-PTB) after treatment with bedaquiline and linezolid. Materials and methods. A clinical and laboratory examination of 175 people with MDR-PTB (89 patients with new cases and 86 patients with recurrent cases of destructive forms of MDR-PTB). The study was performed before and after treatment with bedaquiline and linezolid. The total leukocytes count (L), the leukocyte differential count (leukocyte formula), was determined in all subjects, The content of populations and subpopulations of lymphocytes were calculated using monoclonal antibodies to CD3+, CD4+, CD8+, CD19+, CD23+, CD56+ lymphocytes antigen in the reaction of indirect immunofluorescence. Quantitative determination of serum immunoglobulins was performed by Manchini radial immunodif­fusion in a gel. The level of circulating immune complexes (CIC) was determined by the spectrophoto­metric method by precipitation in polyethylene glycol. Results and discussion. In patients with new cases of destructive forms of MDR-PTB to treatment revealed hypersensitivity reactions of the first and the fourth type. Expressed activation of humoral and killer parts of immunity detected. In patients with recurrent cases of destructive forms of MDR-PTB before treatment, there are pronounced hypersensitivity reactions of the fourth type and activation of the humoral and killer parts of the immune system.Patients with new cases of destructive forms of MDR-PTB after application of treatment regimens with bedaquiline and linezolid have hypersensitivity reactions of the first and fourth types. Activation of humo­ral and killer parts of immunity detected. In patients with recurrent cases of destructive forms of MDR-PTB after the application of treatment regimens with bedaquiline and linezolid revealed a pronounced hypersensitivity reaction of the first type and activation of the killer and humoral parts of the immune system. Conclusions. In patients with new cases of destructive forms of MDR-PTB before treatment revealed T-cell immunodeficiency, which is expressed by a decrease in the level of T-lymphocytes (1.7 times relative to normal) and T-helpers (twice below normal). In patients with recurrent cases of destructive forms of MDR-PTB before treatment revealed T-cell immunodeficiency with a marked decrease in the level of T-lymphocytes (1.8 times normal) and T-helpers (1.8 times below normal). In patients with new cases of destructive forms of MDR-PTB after the application of treatment regimens with bedaquiline and linezolid revealed activation of the T-cell immune system due to increased levels of T-suppressors. In patients with recurrent cases of destructive forms of MDR-PTB after the application of treatment regimens with bedaquiline and linezolid revealed T-cell immunodeficiency due to the reduced content of T-lymphocytes (1.5 times below normal), namely T-helpers (1.9 times lower than normal).

scholarly journals Productive Infection of Neonatal CD8+ T Lymphocytes by HIV-1

1998 ◽  
Vol 187 (7) ◽  
pp. 1139-1144 ◽  
Author(s):  
Liang Peng Yang ◽  
James L. Riley ◽  
Richard G. Carroll ◽  
Carl H. June ◽  
James Hoxie ◽  
...  
Keyword(s):  
T Cells ◽  
Immune System ◽  
T Cell ◽  
T Lymphocytes ◽  
Hiv Infection ◽  
Cd8 T Cells ◽  
Productive Infection ◽  
Target Cells ◽  
Cd8 T Lymphocytes ◽  
Hiv 1

CD8+ T lymphocytes confer significant but ultimately insufficient protection against HIV infection. Here we report that activated neonatal CD8+ T cells can be productively infected in vitro by macrophage-tropic (M-tropic) HIV-1 isolates, which are responsible for disease transmission, whereas they are resistant to T cell–tropic (T-tropic) HIV strains. Physiological activation of CD8-α/β+ CD4− T cell receptor–α/β+ neonatal T cells, including activation by allogeneic dendritic cells, induces the accumulation of CD4 messenger RNA and the expression of CD4 Ag on the cell surface. The large majority of anti-CD3/B7.1–activated cord blood CD8+ T cells coexpress CD4, the primary HIV receptor, as well as CCR5 and CXCR4, the coreceptors used by M- and T-tropic HIV-1 strains, respectively, to enter target cells. These findings are relevant to the rapid progression of neonatal HIV infection. Infection of primary HIV-specific CD8+ T cells may compromise their survival and thus significantly contribute to the failure of the immune system to control the infection. Furthermore, these results indicate a previously unsuspected level of plasticity in the neonatal immune system in the regulation of CD4 expression by costimulation.

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