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Jessica L. Rojas Restrepo

Name	Jessica L. Rojas Restrepo
Place	Deutschland Kolumbien
Gender	weiblich
Variant	Jessica Lineth Rojas Restrepo Jessica Lineth Rojas Restrepo Jessica Rojas
Related	Biomedizin (Studienfach)
Further information	2019: Centrum für Chronische Immundefizienz - CCI, Freiburg
Source	FreiDok plus
Record type	Person
GND-Identifier	1182722385
Record ID	1182722385
Involved in show all Correction to: Functional relevance of CTLA4 variants: an upgraded approach to assess CTLA4‑dependent transendocytosis by flow cytometry Functional relevance of CTLA4 variants: an upgraded approach to assess CTLA4-dependent transendocytosis by flow cytometry Genetic analysis of a cohort of 275 patients with hyper-IgE syndromes and/or chronic mucocutaneous candidiasis Pembrolizumab for treatment of progressive multifocal leukoencephalopathy in primary immunodeficiency and/or hematologic malignancy: a case series of five patients Establishing the molecular diagnoses in a cohort of 291 patients with predominantly antibody deficiency by targeted next-generation sequencing: Experience from a monocentric study Clinical and immunological phenotype of patients with primary immunodeficiency due to damaging mutations in NFKB2

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Jessica L. Rojas Restrepo

Correction to: Functional relevance of CTLA4 variants: an upgraded approach to assess CTLA4‑dependent transendocytosis by flow cytometry

Functional relevance of CTLA4 variants: an upgraded approach to assess CTLA4-dependent transendocytosis by flow cytometry

Genetic analysis of a cohort of 275 patients with hyper-IgE syndromes and/or chronic mucocutaneous candidiasis

Pembrolizumab for treatment of progressive multifocal leukoencephalopathy in primary immunodeficiency and/or hematologic malignancy: a case series of five patients

Establishing the molecular diagnoses in a cohort of 291 patients with predominantly antibody deficiency by targeted next-generation sequencing: Experience from a monocentric study

Clinical and immunological phenotype of patients with primary immunodeficiency due to damaging mutations in NFKB2