Connor Cole

ORCID: 0000-0003-4641-0104
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About
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Research Areas
  • Autoimmune Bullous Skin Diseases
  • Urticaria and Related Conditions
  • Coagulation, Bradykinin, Polyphosphates, and Angioedema
  • Platelet Disorders and Treatments
  • Ocular Infections and Treatments
  • Fungal Infections and Studies
  • Dermatology and Skin Diseases
  • Cutaneous lymphoproliferative disorders research
  • Eosinophilic Disorders and Syndromes
  • Cell Adhesion Molecules Research
  • Antifungal resistance and susceptibility

Rush University Medical Center
2022-2024

Princess Margaret Hospital for Children
2012

Pathwest Laboratory Medicine
2012

The University of Western Australia
2012

Introduction Inflammatory epidermolysis bullosa acquisita (EBA) is characterized by a neutrophilic response to anti-type VII collagen (COL7) antibodies resulting in the development of skin inflammation and blistering. The antibody transfer model EBA closely mirrors this phenotype. Methods To better understand changes induced neutrophils upon recruitment from peripheral blood into lesional EBA, we performed single-cell RNA-sequencing whole dissociate capture minimally perturbed characterize...

10.3389/fimmu.2023.1266359 article EN cc-by Frontiers in Immunology 2023-09-20

Abstract While autoantibodies in bullous pemphigoid (BP) are known to activate the innate immune response, their direct effect on keratinocytes, and contribution of BP-IgG autoantibody-dependent keratinocyte responses BP pathology is largely unknown. Herein, we performed multiplex immunoassays bulk RNA-seq primary keratinocytes treated with IgG from patients or controls. We identified a pro-inflammatory proteolytic response release several cytokines (IL-6, IL-24, TGF-β1), chemokines (CXCL16,...

10.1101/2024.10.07.616103 preprint EN bioRxiv (Cold Spring Harbor Laboratory) 2024-10-11

10.1007/s13671-022-00369-2 article EN Current Dermatology Reports 2022-09-02

Das bullöse Pemphigoid ist eine blasenbildende Autoimmunerkrankung, die durch Autoantikörper verursacht wird, auf BP180 und BP230 abzielen. Während Ablagerungen von IgG und/oder Komplement entlang der epidermalen Basalmembran typischerweise komplementvermittelte Pathogenese hindeuten, weisen mehrere neuere Erkenntnisse komplementunabhängige Wege hin, zu Gewebeschäden subepidermaler Blasenbildung beitragen. Die wesentlichen umfassen Makropinozytose IgG-BP180-Komplexen, einer Depletion...

10.1159/000527569 article DE Kompass Dermatologie 2022-01-01
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