Dr. med. Petra Reis

@article{pmid39874224,

title = {CD19-CAR T-cell therapy induces deep tissue depletion of B cells},

author = {Carlo Tur and Markus Eckstein and Joachim Velden and Simon Rauber and Christina Bergmann and Janina Auth and Laura Bucci and Giulia Corte and Melanie Hagen and Andreas Wirsching and Ricardo Grieshaber-Bouyer and Petra Reis and Nicolai Kittan and Jochen Wacker and Aleix Rius Rigau and Andreas Ramming and Maria-Antonietta D'Agostino and Arndt Hartmann and Fabian Müller and Andreas Mackensen and Aline Bozec and Georg Schett and Maria Gabriella Raimondo},

doi = {10.1136/ard-2024-226142},

issn = {1468-2060},

year  = {2025},

date = {2025-01-01},

journal = {Ann Rheum Dis},

volume = {84},

number = {1},

pages = {106–114},

abstract = {OBJECTIVES: CD19-targeting chimeric antigen receptor (CAR) T-cell therapy can induce long-term drug-free remission in patients with autoimmune diseases (AIDs). The efficacy of CD19-CAR T-cell therapy is presumably based on deep tissue depletion of B cells; however, such effect has not been proven in humans in vivo. 

METHODS: Sequential ultrasound-guided inguinal lymph node biopsies were performed at baseline and after CD19-CAR T-cell therapy in patients with AIDs. Results were compared with lymph node biopsies from rituximab (RTX)-treated AID patients with absence of peripheral B cells. Conventional and immunohistochemistry staining were performed on lymph node tissue to assess architecture as well the number of B cells, follicular dendritic cells (FDCs), plasma cells, T cells and macrophages. 

RESULTS: Sequential lymph node biopsies were analysed from five patients with AID before and after CD19-CAR T-cell therapy and from five patients with AID after RTX treatment. In addition, non-lymphoid organ biopsies (colon, kidney and gallbladder) from three additional patients with AID after CD19-CAR T-cell therapy were analysed. CD19 and CD20 B cells were completely depleted in the lymph nodes after CD19-CAR T-cell therapy, but not after RTX treatment. Plasma cells, T cells and macrophages in the lymph nodes remained unchanged. Follicular structures were disrupted and FDCs were depleted in the lymph nodes after CD19-CAR T-cell therapy, but not after RTX. Non-lymphoid organs were completely depleted of B cells. 

DISCUSSION: This study demonstrates complete B-cell depletion in secondary lymphoid tissues of patients with AIDs following CD19-CAR T-cell therapy combined with standard lymphodepleting therapy.},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{pmid36704900,

title = {Clinical Images: Increased bone metabolism in secondary hyperparathyroidism},

author = {Larissa Valor-Méndez and Armin Atzinger and Petra Reis and Bernhard Manger and Georg Schett},

doi = {10.1002/art.42458},

issn = {2326-5205},

year  = {2023},

date = {2023-06-01},

journal = {Arthritis Rheumatol},

volume = {75},

number = {6},

pages = {1072},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{pmid25026959,

title = {IgG4- related disease: an orphan disease with many faces},

author = {Herwig Pieringer and Ilse Parzer and Adelheid Wöhrer and Petra Reis and Bastian Oppl and Jochen Zwerina},

doi = {10.1186/s13023-014-0110-z},

issn = {1750-1172},

year  = {2014},

date = {2014-07-01},

journal = {Orphanet J Rare Dis},

volume = {9},

pages = {110},

abstract = {Immunoglobulin G4- related disease (IgG4-RD) is a rare systemic fibro-inflammatory disorder (ORPHA284264). Although patients have been described more than 100 years ago, the systemic nature of this disease has been recognized in the 21st century only. Type 1 autoimmune pancreatitis is the most frequent manifestation of IgG4-RD. However, IgG4-RD can affect any organ such as salivary glands, orbits, retroperitoneum and many others. Recent research enabled a clear clinical and histopathological description of IgG4-RD. Typically, lymphoplasmacellular inflammation, storiform fibrosis and obliterative phlebitis are found in IgG4-RD biopsies and the tissue invading plasma cells largely produce IgG4. Elevated serum IgG4 levels are found in many but not all patients. Consequently, diagnostic criteria for IgG4-RD have been proposed recently. Treatment is largely based on clinical experience and retrospective case series. Glucocorticoids are the mainstay of therapy, although adjunctive immunosuppressive agents are used in relapsing patients. This review summarizes current knowledge on clinical manifestations, pathophysiology and treatment of IgG4-RD.},

keywords = {},

pubstate = {published},

tppubtype = {article}

}