Limary Medina

ORCID: 0000-0003-3214-7616
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About
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Research Areas
  • Psoriasis: Treatment and Pathogenesis
  • T-cell and B-cell Immunology
  • Dermatology and Skin Diseases
  • Monoclonal and Polyclonal Antibodies Research
  • Immune Cell Function and Interaction
  • Immunodeficiency and Autoimmune Disorders
  • Autoimmune Bullous Skin Diseases
  • Microbial infections and disease research
  • Pharmacological Effects of Natural Compounds
  • Cytokine Signaling Pathways and Interactions
  • Viral Infectious Diseases and Gene Expression in Insects
  • Respiratory viral infections research
  • Pediatric health and respiratory diseases
  • Urticaria and Related Conditions
  • CAR-T cell therapy research

AbbVie (United States)
2013-2021

AbbVie (Japan)
2013

Massachusetts Academy of Math and Science
2013

University of Illinois Chicago
1994

Abstract IL-36 cytokines are pro-inflammatory members of the IL-1 family that upregulated in inflammatory disorders. Specifically, IL-36γ is highly expressed active psoriatic lesions and can drive processes 3D human skin equivalents supporting a role for this target inflammation. Small molecule antagonists interleukins have been historically challenging to generate. Nevertheless, we performed small high-throughput screen identify using novel TR-FRET binding assay. Several compounds,...

10.1038/s41598-019-45626-w article EN cc-by Scientific Reports 2019-06-24

Signal transduction through the interleukin-1 receptor (IL-1R) pathway mediates a strong pro-inflammatory response, which contributes to number of human diseases such as rheumatoid arthritis. Within IL-1 family, IL-1α and IL-1β are both agonistic ligands for IL-1R, whereas antagonist (IL-1ra) is an endogenous that binds IL-R, but does not signal. Therefore, ideal therapeutic strategy would be blocking IL-1β, IL-1ra. However, due low sequence homology between three members it has been...

10.4161/mabs.1.4.8755 article EN mAbs 2009-08-01

IL-36 cytokines signal through the receptor (IL-36R) and a shared subunit, IL-1RAcP (IL-1 accessory protein). The activation mechanism for pathway is proposed to be similar that of IL-1 in an IL-36R agonist (IL-36α, IL-36β, or IL-36γ) forms binary complex with IL-36R, which then recruits IL-1RAcP. Recent studies have shown interacts even absence agonist. To elucidate mechanism, we considered all possible binding events ligands/receptors examined these direct assays. Our results indicated...

10.1074/jbc.m117.805739 article EN cc-by Journal of Biological Chemistry 2017-11-27

Abstract CTLA4-Ig/abatacept dampens activation of naive T cells by blocking costimulation via CD28. It is an approved drug for rheumatoid arthritis but failed to deliver efficacy in a number other autoimmune diseases. One explanation that activated rely less on CD28 signaling and use alternate coreceptors effector function. ICOS critical T-dependent humoral immune responses, which drives pathophysiology IgG-mediated In this study, we asked whether play nonredundant roles maintenance...

10.4049/jimmunol.2001100 article EN The Journal of Immunology 2021-01-25

Efficient production of large quantities therapeutic antibodies is becoming a major goal the pharmaceutical industry. We developed proprietary expression system using polyprotein precursor-based approach to antibody in mammalian cells. In this approach, coding regions for heavy and light chains are included within single open reading frame (sORF) separated by an in-frame intein gene. A mRNA subsequent polypeptide produced upon transient stable transfection into HEK293 CHO cells,...

10.4161/mabs.25161 article EN mAbs 2013-05-31
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