Sarah M Volkers1, Christian Meisel2,3, Dorothea Terhorst-Molawi4, Guido J Burbach5, Dirk Schürmann1, Norbert Suttorp1,6, Leif E Sander7,8. 1. Department of Infectious Diseases and Respiratory Medicine, Charité-Universitätsmedizin Berlin, corporate member of Freie Universität Berlin, Humboldt-Universität zu Berlin, and Berlin Institute of Health, Berlin, Germany. 2. Institute of Medical Immunology, Charité-Universitätsmedizin Berlin, corporate member of Freie Universität Berlin, Humboldt-Universität zu Berlin, and Berlin Institute of Health, Berlin, Germany. 3. Department of Immunology, Labor Berlin-Charité Vivantes GmbH, Berlin, Germany. 4. Department of Dermatology, Charité-Universitätsmedizin Berlin, corporate member of Freie Universität Berlin, Humboldt-Universität zu Berlin, and Berlin Institute of Health, Berlin, Germany. 5. Dermatology/Dermato-Oncology Out-Patient Clinic, Vivantes Ambulatory Health Care Centers Berlin-Spandau, Berlin, Germany. 6. German Center for Lung Research (DZL), Berlin, Germany. 7. Department of Infectious Diseases and Respiratory Medicine, Charité-Universitätsmedizin Berlin, corporate member of Freie Universität Berlin, Humboldt-Universität zu Berlin, and Berlin Institute of Health, Berlin, Germany. leif-erik.sander@charite.de. 8. German Center for Lung Research (DZL), Berlin, Germany. leif-erik.sander@charite.de.
Abstract
BACKGROUND: Erythema multiforme (EM) is an acute, immune-mediated mucocutaneous disease, most often preceded by herpes simplex virus (HSV) infection or reactivation. Mycoplasma pneumoniae (Mp) is considered the second major trigger of EM and is often associated with an atypical and more severe presentation of disease, characterized by prominent mucosal involvement. However, contrary to HSV-associated Erythema multiforme (HAEM), immunological mechanisms of Mp-associated EM remain unclear. CASE PRESENTATION: We present the case of a 50-year-old male patient presenting with community-acquired pneumonia (CAP) and erythema multiforme majus (EMM). Acute Mp infection was diagnosed by seroconversion, with no evidence of HSV infection as a cause of EMM. We performed immune phenotyping of blister fluid (BF) and peripheral blood (PB) T cells and detected a clonally expanded TCRVβ2+ T cell population that was double positive for CD4 and CD8, and expressed the cytotoxic markers granulysin and perforin. This CD4+CD8+ population comprised up to 50.7% of BF T cells and 24.9% of PB T cells. Two years prior to the onset of disease, the frequency of PB CD4+CD8+T cells had been within normal range and it gradually returned to baseline levels with the resolution of symptoms, suggesting an involvement of this population in EMM disease pathophysiology. CONCLUSIONS: This report is the first to provide a phenotypic description of lesional T cells in Mp-associated EMM. Characterizing the local immune response might help to address pathophysiological questions and warrants further systematic research.
BACKGROUND:Erythema multiforme (EM) is an acute, immune-mediated mucocutaneous disease, most often preceded by herpes simplex virus (HSV) infection or reactivation. Mycoplasma pneumoniae (Mp) is considered the second major trigger of EM and is often associated with an atypical and more severe presentation of disease, characterized by prominent mucosal involvement. However, contrary to HSV-associated Erythema multiforme (HAEM), immunological mechanisms of Mp-associated EM remain unclear. CASE PRESENTATION: We present the case of a 50-year-old male patient presenting with community-acquired pneumonia (CAP) and erythema multiforme majus (EMM). Acute Mp infection was diagnosed by seroconversion, with no evidence of HSV infection as a cause of EMM. We performed immune phenotyping of blister fluid (BF) and peripheral blood (PB) T cells and detected a clonally expanded TCRVβ2+ T cell population that was double positive for CD4 and CD8, and expressed the cytotoxic markers granulysin and perforin. This CD4+CD8+ population comprised up to 50.7% of BF T cells and 24.9% of PB T cells. Two years prior to the onset of disease, the frequency of PB CD4+CD8+T cells had been within normal range and it gradually returned to baseline levels with the resolution of symptoms, suggesting an involvement of this population in EMM disease pathophysiology. CONCLUSIONS: This report is the first to provide a phenotypic description of lesional T cells in Mp-associated EMM. Characterizing the local immune response might help to address pathophysiological questions and warrants further systematic research.
Entities:
Keywords:
CD4+ CD8+ double-positive T cells; Erythema multiforme; Mucosal-associated invariant T cells; Mycoplasma pneumoniae-associated rash and mucositis; T cells; T effector memory RA+ T cells; Tissue-resident memory T cells
Authors: L Flamand; R W Crowley; P Lusso; S Colombini-Hatch; D M Margolis; R C Gallo Journal: Proc Natl Acad Sci U S A Date: 1998-03-17 Impact factor: 11.205
Authors: Ren-You Pan; Mu-Tzu Chu; Chuang-Wei Wang; Yun-Shien Lee; Francois Lemonnier; Aaron W Michels; Ryan Schutte; David A Ostrov; Chun-Bing Chen; Elizabeth Jane Phillips; Simon Alexander Mallal; Maja Mockenhaupt; Teresa Bellón; Wichittra Tassaneeyakul; Katie D White; Jean-Claude Roujeau; Wen-Hung Chung; Shuen-Iu Hung Journal: Nat Commun Date: 2019-08-08 Impact factor: 14.919