Jacek M. Witkowski

ORCID: 0000-0003-2906-1109
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About
Contact & Profiles
Research Areas
  • Immune Cell Function and Interaction
  • T-cell and B-cell Immunology
  • Neuroinflammation and Neurodegeneration Mechanisms
  • Tryptophan and brain disorders
  • Immune responses and vaccinations
  • Alzheimer's disease research and treatments
  • Immunotherapy and Immune Responses
  • Astro and Planetary Science
  • Calpain Protease Function and Regulation
  • Systemic Lupus Erythematosus Research
  • Genetics, Aging, and Longevity in Model Organisms
  • Antimicrobial Resistance in Staphylococcus
  • Monoclonal and Polyclonal Antibodies Research
  • Drug Transport and Resistance Mechanisms
  • Neutrophil, Myeloperoxidase and Oxidative Mechanisms
  • Inflammasome and immune disorders
  • Diabetes and associated disorders
  • Gut microbiota and health
  • Cytomegalovirus and herpesvirus research
  • Erythropoietin and Anemia Treatment
  • Lipid Membrane Structure and Behavior
  • Neuroscience and Neuropharmacology Research
  • Rheumatoid Arthritis Research and Therapies
  • Immunodeficiency and Autoimmune Disorders
  • RNA regulation and disease

Gdańsk Medical University
2016-2025

University of Gdańsk
1992-2023

PES University
2023

Université de Sherbrooke
2021

Jagiellonian University
2021

Oxford University Hospitals NHS Trust
2010

University of Regensburg
2010

National Institute of Biomedical Innovation, Health and Nutrition
2010

Research Institute of General Pathology and Pathophysiology, the Russian Academy of Medical Sciences
2005-2010

Jan Długosz University
2008

Abstract The ability to mount protective immune responses depends on the diversity of T cells. cell may be compromised by declining thymic output new aging process imposes a threat diversity, because function deteriorates. In this study we have examined relationship between production, homeostatic proliferation and TCR β-chain in young (∼25 years), middle-aged (∼60 elderly adults (∼75 years). excision circles (TREC) as marker exponentially decreased >95% 25 60 years age. frequency...

10.4049/jimmunol.174.11.7446 article EN The Journal of Immunology 2005-06-01

The distribution of peripheral T cell subsets in young and healthy old people is markedly different, characterized by decreased numbers naïve cells increased clonal expansions memory cells, predominantly the CD8+ MHC class I-restricted subset. Here, however, we document dramatic alterations CD4+ patients with mild Alzheimer's disease (AD), greatly percentages elevated proportions but not lacking important costimulatory receptor CD28. CD4+CD25(high) potentially regulatory a phenotype are also...

10.3233/jad-2009-1015 article EN Journal of Alzheimer s Disease 2009-05-26

Senile amyloid plaques are one of the main hallmarks Alzheimer's disease (AD). They correspond to insoluble deposits amyloid-β peptides (Aβ) and responsible for inflammatory response neurodegeneration that lead loss memory. Recent data suggest Aβ possess antimicrobial a nd anti-viral activity in vitro. Here, we have used cocultures neuroglioma (H4) glioblastoma (U118-MG) cells as minimal vitro model investigate whether is produced by this could result protective against HSV-1 infection....

10.3233/jad-150652 article EN Journal of Alzheimer s Disease 2016-02-22

Alzheimer's disease (AD) is the most common neurodegenerative ultimately manifesting as clinical dementia. Despite considerable effort and ample experimental data, role of neuroinflammation related to systemic inflammation still unsettled. While implication microglia well recognized, exact contribution peripheral monocytes/macrophages largely unknown, especially concerning their in various stages AD.AD develops over decades its manifestation preceded by subjective memory complaints (SMC)...

10.1186/s12979-021-00236-x article EN cc-by Immunity & Ageing 2021-06-21

Abstract Objective The immune system of patients with rheumatoid arthritis (RA) is characterized by the accumulation CD4+ T cells deficient in CD28 expression and up‐regulation tumor necrosis factor α (TNFα). Previous vitro studies have shown that TNFα induces transcriptional silencing gene. Because reduced compromises immunocompetence, we examined whether RA vivo reduction related to TNFα. Methods Patients age‐matched individuals were recruited. Peripheral blood mononuclear stained for CD3,...

10.1002/art.21353 article EN Arthritis & Rheumatism 2005-09-30
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