Lourdes Baranda

Roche (Switzerland)

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Roberto González‐Amaro

Autonomous University of San Luis Potosí

Carlos Abud‐Mendoza

Autonomous University of San Luis Potosí

Diana Patricia Portales‐Pérez

Autonomous University of San Luis Potosí

Esther Layseca‐Espinosa

Autonomous University of San Luis Potosí

Bertha Torres‐Álvarez

Autonomous University of San Luis Potosí

Perla Niño-Moreno

Autonomous University of San Luis Potosí

Adriana Monsiváis‐Urenda

Autonomous University of San Luis Potosí

Hortensia de la Fuente

Centro de Investigación en Red en Enfermedades Cardiovasculares

Berenice Hernández-Castro

Autonomous University of San Luis Potosí

B Moncada

Sleep Research Society

Cooperative Institutions

Autonomous University of San Luis Potosí

Hospital Central Dr. Ignacio Morones Prieto

Universidad Nacional Autónoma de México

Polytechnic University of San Luis Potosí

Universidad Autónoma de Madrid

Instituto Nacional de Ciencias Médicas y Nutrición Salvador Zubirán

Hospital Universitario de La Princesa

Mexican Social Security Institute

Roche (Switzerland)

Universidad Complutense de Madrid

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CTLA-4-Ig Therapy Diminishes the Frequency but Enhances the Function of Treg Cells in Patients with Rheumatoid Arthritis

Journal of Clinical Immunology (2011)

Crisol Álvarez-Quiroga Carlos Abud‐Mendoza Lesly Doníz-Padilla Amida Juárez-Reyes Adriana Monsiváis‐Urenda

Abatacept

CTLA-4

Regulatory T cell

10.1007/s10875-011-9527-5

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Citations (102)

Lack of involvement of P-glycoprotein (P-gp) in pemphigus patients with poor response to steroid therapy

Journal of Dermatological Science (2002)

Hortensia de la Fuente Lourdes Baranda Martha Hernandez Bertha Torres‐Álvarez Luis Llorente

P-glycoprotein

Pemphigus vulgaris

10.1016/s0923-1811(01)00169-4

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Citations (3)

Expression and function of IL‐10R in mononuclear cells from patients with systemic lupus erythematosus

Scandinavian Journal of Rheumatology (2006)

Guillermo Valencia‐Pacheco Esther Layseca‐Espinosa Perla Niño-Moreno Diana Patricia Portales‐Pérez Lourdes Baranda

Objective: To assess the expression and function of the receptor for interleukin‐10 (IL‐10R) in immune cells from patients with systemic lupus erythematosus (SLE).Methods: We assessed the expression and function of IL‐10R in peripheral blood mononuclear cells (PBMCs) from 19 SLE patients and 15 healthy controls. The expression of IL‐10R was assessed by flow cytometry, and the function of this receptor was determined by analysing both the activation of Jak‐1, Tyk‐2, Stat‐1, and Stat‐3 (Western blot) and the induction of gene expression (cDNA array test of 242 genes of cytokines, apoptosis and intracellular signalling) upon stimulation with IL‐10.Results: We found similar levels of IL‐10R expression in SLE patients and controls. In addition, variable levels of Jak‐1, Tyk‐2, Stat‐1, and Stat‐3 activation were induced by IL‐10 in PBMCs from SLE patients and controls, with no significant differences in protein phosphorylation or kinetics of activation. However, clear‐cut differences in the gene expression induced through IL‐10R were observed in SLE patients and controls, mainly in the genes involved in apoptosis and those encoding for cytokines and their receptors.Conclusions: Our data suggest that despite normal levels of IL‐10R expression, and an apparent lack of abnormalities in the intracellular signals induced through this receptor, immune cells from SLE patients exhibit an aberrant pattern of gene expression induced through the IL‐10R.

10.1080/03009740600709840

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Citations (13)

AB0043 Regulatory Function of Natural Killer Cells in Systemic Lupus Erythematosus (SLE)

Annals of the Rheumatic Diseases (2014)

Daniela de Jesús Cruz-González Yael Sebastián Villaseñor-Talavera Lourdes Baranda Roberto González‐Amaro A.E. Monsivais Urenda

Background

Natural killer (NK) cells are large granular lymphocytes that belong to the innate immunity. The activation or inhibition of NK cells is regulated by several membrane receptors, commonly designated as NK cell receptors (NKR). Despite its well-known functions it has been recently reported that NK cells are also involved in the regulation of the adaptive immune response. The NK regulatory mechanisms include the acquisition of MHC class II and costimulatory molecules to sub-optimal levels in order to induce T cell anergy. Moreover, it has been found that NK cells are able to inhibit T cell proliferation by lysing dendritic cells (DC). Systemic lupus erythematosus (SLE) is an autoimmune disease, which results from numerous immunological abnormalities. It has been described that SLE patients display impairment in both, the levels and the cytotoxic function of NK cells. However, NK cells regulatory function in SLE has not been evaluated.

Objectives

We aim to study the NKR and costimulatory molecules expression in NK cells from SLE patients, as well as its inhibitory function.

Methods

Fifteen SLE patients according to the classification criteria of the American College of Rheumatology and seven healthy controls have been included. The expression of NKG2D, NKG2C, NKG2A, NKp46, NKp30, ILT2, CD161, and costimulatory molecules: CD80, CD86, HLA-DR, CD134 (OX40), was evaluated in peripheral blood NK cells (CD3-CD56+) by multiparametric flow cytometry. In order to evaluate the inhibitory function of NK cells, we performed co-cultures with NK cells and autologous, CFSE loaded, immature DC or mature DC as targets cells; co-cultures were done at different NK cells–DC ratios (0:1, 1:5, 5:1, 1:0) for 24h and 48 h; the percentage of DC lysis was assessed by flow cytometry.

Results

We found that SLE patients show a similar pattern of NKR expression than healthy controls. However, the inhibitory receptor ILT2 and the activator NKR, NKp30 and NKG2C, showed a slight increase in their expression. Furthermore, we observed that the expression of the costimulatory molecules CD80, CD86 and CD134, as well as HLA-DR was increased in SLE patients compared to healthy controls. In addition, we found that NK from SLE patients are less capable to lyse immature DC compared with control NK cells. In contrast, NK cells from SLE patients are more efficient lysing mature DC compared with controls.

Conclusions

Our results suggest that NK cells from SLE patients show an activating phenotype, which, in addition to the high expression of HLA-DR and costimulatory molecules provides them with the ability to present antigens and activate T cells. Furthermore, NK cells from SLE patients do not lyse immature DC efficiently, which may promote the presentation of auto-antigens by DC resulting in the activation of autoreactive T cells. All the above may contribute to SLE pathogenesis.

References

Novel APC-like properties of human NK cells directly regulate T cell activation. Hanna J, et al. J Clin Invest 2004; 114:1612-1623. Natural killer (NK)–dendritic cell interactions generate MHC class II-dressed NK cells that regulate CD4+ T cells. Nakayama M, et al. PNAS, 2011 108:18360–18365.

Disclosure of Interest

None declared

DOI

10.1136/annrheumdis-2014-eular.4519

CD86

CD80

Janus kinase 3

NKG2D

10.1136/annrheumdis-2014-eular.4519

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Citations (0)

1270P IMscin001: Phase Ib dose-finding study of subcutaneous atezolizumab in patients with locally advanced or metastatic non-small cell lung cancer (NSCLC)

Annals of Oncology (2020)

Mauricio Burotto Enriqueta Felip Zanete Zvirbule Lourdes Baranda Pascal Chanu

Atezolizumab

10.1016/j.annonc.2020.08.1584

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Proportions of several types of plasma and urine microparticles are increased in patients with rheumatoid arthritis with active disease

Clinical & Experimental Immunology (2015)

Verónica Viñuela‐Berni Lesly Doníz-Padilla Nicté Figueroa‐Vega Haydée Portillo-Salazar Carlos Abud‐Mendoza

We analysed the proportions of different microparticles (MPs) in plasma from patients with rheumatoid arthritis (RA), and assessed their relationship with disease activity/therapy and their in-vitro effect on proinflammatory cytokine release. Blood and urine samples were obtained from 55 patients with RA (24 untreated and 31 under conventional therapy) and 20 healthy subjects. Fourteen patients with systemic lupus erythematosus (SLE) were also studied. The proportions of CD3(+) , CD14(+) , CD19(+) , CD41(+) and CD62E(+) MPs were determined by flow cytometry analysis. The in-vitro effect of plasma MPs on the release of interleukin (IL)-1, IL-6, IL-17 and tumour necrosis factor (TNF)-α was also analysed. We detected that the proportions of different types of annexin-V(+) MPs were enhanced in plasma (CD3(+) , CD14(+) , CD19(+) , CD41(+) and CD62E(+) MPs) and urine (CD14(+) , CD3(+) and CD19(+) MPs) from RA patients with high disease activity (DAS28 index > 5·1). Accordingly, a significant positive correlation was observed between the levels of MPs and DAS28 score, and these levels diminished significantly at week 4 of immunosuppressive therapy. Finally, MPs isolated from patients with high disease activity induced, in vitro, an enhanced release of IL-1, IL-17 and TNF-α. In SLE, enhanced levels of different types of plasma MPs were also detected, with a tight correlation with disease activity. Our data further support that MPs have a relevant role in the pathogenesis of RA and suggest that the analysis of the proportions of these microvesicles in plasma could be useful to monitor disease activity and therapy response in patients with RA.

Proinflammatory cytokine

Pathogenesis

10.1111/cei.12598

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Citations (53)

Magnetic resonance imaging in patients with rheumatoid arthritis with complete remission treated with disease-modifying antirheumatic drugs or anti-tumour necrosis factor agents

Annals of the Rheumatic Diseases (2006)

Marco Ulises Martínez‐Martínez Enrique Cuevas-Orta G Reyes-Vaca Lourdes Baranda Roberto González‐Amaro

with ankylosing spondylitis ATI developed within 24 weeks in association with undetectable serum trough infliximab levels, inefficacy of infliximab and infusion reactions.The number of patients, however, is too small to draw definite conclusions, but interestingly, these data point in the same direction as described previously in rheumatoid arthritis. 3 Lower serum trough infliximab levels could be explained by enhanced clearance because of immune complex formation between anti-infliximab antibodies and infliximab.To prevent ATI formation that might inhibit the efficacy of infliximab, it might be helpful to increase the dosage of infliximab (as occurs in treatment of rheumatoid arthritis with infliximab), to shorten the interval between infliximab infusions (as is currently the strategy in Crohn's disease) or to provide coadministration of other immunosuppressives (such as methotrexate).These data should be confirmed in a larger group of patients with ankylosing spondylitis to develop a more patient-specific treatment, which might predict the inefficacy of infliximab at an early stage and might prevent adverse reactions.

Antirheumatic drugs

10.1136/ard.2006.056432

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Citations (11)

Expression of CD64 as a potential marker of neonatal sepsis

Pediatric Allergy and Immunology (2002)

Esther Layseca‐Espinosa Luis Fernando Pérez-González Abraham Torres‐Montes Lourdes Baranda Hortensia de la Fuente

The aim of this study was to identify a novel immunological indicator useful for the early diagnosis (through a rapid and single determination) of neonatal sepsis (NS). Peripheral blood samples were taken from 63 neonates, who were classified into four groups: proven NS (n = 17); clinical NS (n = 14); disease without infection (n = 17); and healthy newborns (n = 15). Neutrophil expression of CD64, CD43, CD44, CD50, CD62L and Mac‐1, and plasma levels of interleukin (IL)‐1β, IL‐6, tumor necrosis factor‐α (TNF‐α) and soluble L ‐selectin (sCD62L), were determined. Expression of CD64 was significantly enhanced in the group with proven sepsis and clinical NS compared to newborns without infection (p < 0.05). Eight newborns with proven or clinical sepsis, but only one with disease without infection, showed an increased percentage of CD64 + cells (diagnostic specificity = 96.8%). No significant differences were found in the expression of the other leucocyte differentiation antigens studied. As previously described, TNF‐α and IL‐6 levels were significantly elevated in newborns with proven or clinical sepsis compared to neonates without infection (p < 0.05). Our results suggest that, through a single determination, the enhanced expression of CD64 is a highly specific indicator of NS, although its diagnostic sensitivity is low (25.8%). In contrast, we found that plasma levels of IL‐1β and sCD62L, as well as the expression of Mac‐1, CD43, CD44, CD50, and CD62L, do not appear to be useful for the diagnosis of NS.

CD64

Neonatal Sepsis

10.1034/j.1399-3038.2002.01064.x

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Citations (94)

Expression and function of the purinergic receptor P2X7 in patients with pulmonary tuberculosis

Clinical & Experimental Immunology (2006)

S Franco-Martínez Perla Niño-Moreno Sofía Bernal‐Silva Lourdes Baranda M Rocha-Meza

Summary P2X7 is a channel receptor gated by adenosine triphosphate (ATP) that is involved in the killing of intracellular mycobacteria. To explore further the role of P2X7 in immunity against Mycobacterium tuberculosis, we studied its expression and function in 19 patients with pulmonary tuberculosis (TB) and 19 healthy contacts. Flow cytometry analysis showed a similar and variable expression of P2X7 in TB patients and healthy subjects. In contrast, P2X7 mARN levels were significantly higher in TB patients. When the function of the P2X7 receptor in peripheral blood mononuclear cells (PBMC) was assessed by the effect of exogenous ATP on apoptosis, the uptake of the fluorescent marker Lucifer yellow or extracellular signal regulated kinase (ERK) phosphorylation, no significant differences were detected in patients and controls. However, mRNA macroarray analysis showed that upon stimulation with ATP, the PBMC from TB patients showed a significant induction of a higher number of cytokine genes (27 of 96), and a lower number of apoptosis genes (20 of 96) compared to healthy controls (17 and 76 genes, respectively). These results suggest that although the PBMC from TB patients do not show apparent abnormalities in the expression of P2X7, and the intracellular signals generated through it, the pattern of gene expression induced by ATP in these cells is different from that found in healthy contacts. This phenomenon suggests a defective function of P2X7 in the immune cells from TB patients, a condition that may contribute to the inability of these patients to eliminate the mycobacteria.

Purinergic Signalling

10.1111/j.1365-2249.2006.03213.x

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Citations (33)

Ketoconazole and gynecomastia

Journal of the American Academy of Dermatology (1982)

Benjamín Moncada Lourdes Baranda

Gynecomastia

10.1016/s0190-9622(82)80263-6

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Citations (3)