Vojtech Thon

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Alokmay Datta

Saha Institute of Nuclear Physics

PROF. OM PRAKASH SINHA

Amity University

ida idayu muhamad

Universiti Teknologi Malaysia - UTM

Nicole Zacharia

University of Akron

Virginie Boucher

CSIC (Consejo Superior de Investigaciones Científicas-Spanish National Research Council)

Muhammad Khusairy Bakri

Washington State University

Stefan Judex

SUNY: Stony Brook University

Miguel Angel Rubio

Universidad Nacional de Educación a Distancia

Branko Matovic

University of Belgrade

Mico Mitrovic

University of Belgrade

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Interleukin-6 May Contribute to Mortality in Parkinson’s Disease Patients: A 4-Year Prospective Study

Parkinson's Disease, 2015

Objectives. The association between abnormal serum immunomarkers and mortality in 53 consecutive ... more Objectives. The association between abnormal serum immunomarkers and mortality in 53 consecutive Parkinson&amp;amp;amp;amp;amp;amp;amp;amp;#39;s disease patients was studied. Materials and Methods. The plasma level of specific inflammatory cytokines was investigated: mannan-binding lectin (MBL), interleukin- (IL-) 6, and tumor necrosis factor-alpha (TNF-α). The baseline serum immunomarkers obtained from patients who died (n = 16) during a four-year follow-up period were compared with the data of patients who survived (n = 37). Results. The baseline level of IL-6 was significantly higher in the deceased patients than in the survivors. Elevated IL-6 levels and age were major independent contributors to disease mortality. Differences between other plasma cytokine level abnormalities were not significant. Conclusion. This study showed that IL-6 elevation may be a marker of increased mortality risk in Parkinson&amp;amp;amp;amp;amp;amp;amp;amp;#39;s disease patients. The inflammation may act in association with other factors and comorbidities in progressive neurodegenerative pathology.

[Intravenous and subcutaneous immunoglobulin therapy]

Epidemiologie, mikrobiologie, imunologie : casopis Spolecnosti pro epidemiologii a mikrobiologii Ceské lékarské spolecnosti J.E. Purkyne, 2013

Patients with agammaglobulinaemia and hypogammaglobulinaemia require immunoglobulin G (IgG) repla... more Patients with agammaglobulinaemia and hypogammaglobulinaemia require immunoglobulin G (IgG) replacement therapy to prevent serious infections. Since the 1950s, therapy with human immune globulin products has been the standard of treatment. Currently, the most common routes of administration of IgG replacement therapy are intravenous (IVIG) or subcutaneous (SCIG). The home therapy may improve the quality of life in patients who require lifelong IgG replacement. The -anti-IgA antibody test identifies the patients with the risk of anaphylactoid reactions in IVIG replacement. The SCIG delivery may be used in patients with anti-IgA antibodies and previous systemic reactions to IVIG.

A defect in the early phase of TCR-mediated T-cell activation in patients with common variable immunodeficiency

Blood

Common variable immunodeficiency (CVID) is characterized by an impairment of specific antibody pr... more Common variable immunodeficiency (CVID) is characterized by an impairment of specific antibody production and a decrease in all or selected Ig isotypes. Abnormalities at the level of the B cells, T cells, and antigen-presenting cells have been described. In the present study, we have focused our attention on T-cell activation in CVID. T cells from 15 of 24 patients failed to respond to recall antigens (eg, tetanus toxoid, Escherichia coli). Of these 15 patients, 11 were studied in detail and showed significantly decreased T-cell proliferative responses and/or decreased interleukin-2 and interferon-gamma production on T-cell receptor-mediated stimulation with recall antigens and superantigens (staphylococcal enterotoxins [SE]); however, T-cell response to mitogens (anti-CD3 monoclonal antibody, phytohemagglutinin) was normal. The defect in interleukin-2 and interferon-gamma release on tetanus toxoid stimulation could also be documented in purified CD4 T cells of the patients and was ...

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