Mariarosa Battarra
Current Organizations / Institutes
The organizations/institutes from the scholar's latest article
Previous Organizations / Institutes
The organizations / institutes from the scholar's other articles in the past ten years
Mariarosa Battarra has a total of 73 co-authors. Here are the top co-authors by number of shared publications:
- Marco Andreani
Laboratorio d'Immunogenetica dei Trapianti IRCCS Ospedale Pediatrico Bambino Gesù Roma Italy
17 shared publications - Jonathan Visentin
CHU de Bordeaux, Laboratoire d'Immunologie et Immunogénétique Hôpital Pellegrin, Place Amélie Raba Léon Bordeaux France
11 shared publications - Marine Cargou
CHU de Bordeaux, Laboratoire d'Immunologie et Immunogénétique Hôpital Pellegrin, Place Amélie Raba Léon Bordeaux France
8 shared publications Gwendaline Guidicelli
CHU de Bordeaux, Laboratoire d'Immunologie et Immunogénétique, Hôpital Pellegrin, Place Amélie Raba Léon, Bordeaux, France
4 shared publicationsElodie Wojciechowski
CHU de Bordeaux, Laboratoire d'Immunologie et Immunogénétique Hôpital Pellegrin, Place Amélie Raba Léon Bordeaux France
3 shared publicationsMarco Andreani
Laboratorio d'Immunogenetica dei Trapianti, IRCCS Ospedale Pediatrico Bambino Gesù, Roma, Italy
3 shared publications
Latest Publications
- Open Access
- 29 June 2026
- Published by Medical Journals Sweden AB in Acta Dermato-Venereologica
- Vol. 106
Distinctive Reactivity to the C-terminal Epitope of BP180 Characterizes Immune Checkpoint Inhibitor–associated Bullous Pemphigoid, and an ELISA Based on the BP180 Ectodomain Enables Prompt Diagnosis in a Subset of Patients
Growing evidence has linked bullous pemphigoid (BP) to immune checkpoint inhibitor (ICI) therapy in cancer treatment. However, the immunological features of ICI-associated BP (ICI-BP) are not yet fully elucidated. In order to characterize the humoral response in ICI BP patients and investigate whether their epitope profile differs from idiopathic BP (IBP), 53 ICI-BP patients were enrolled, immunologically characterized and compared with 59 IBP patients. ICI-BP had a distinctive IgG humoral profile, with reduced reactivity toward BP230 and recognition of multiple BP180 epitopes beyond the immunodominant extracellular noncollagenous 16A domain (NC16A). Specifically, reactivity to BP180 ectodomain was present in 94% of ICI-BP and 78% of IBP (p=0.044). Moreover, BP180 C-terminal epitope was more frequently targeted in ICI-BP than IBP (72% vs 41%, p=0.002). Notably, the combined use of an in-house BP180 ectodomain ELISA and the commercial BP180 test increased diagnostic sensitivity from 83% to 100%. Enhanced IgG reactivity toward nonimmunodominant epitopes, and especially C-terminal epitope recognition, characterize the humoral immune response in ICI-BP. Our data suggest that combining NC16A and fulllength BP180 ectodomain ELISAs may help reduce diagnostic delay in ICI-BP patients, in whom a timely diagnosis is crucial to appropriately manage the disease and ultimately avoid discontinuation ofcancer therapy.
- 29 June 2026
- Published by Medical Journals Sweden AB in Acta Dermato-Venereologica
- Vol. 106
Open AccessDistinctive Reactivity to the C-terminal Epitope of BP180 Characterizes Immune Checkpoint Inhibitor–associated Bullous Pemphigoid, and an ELISA Based on the BP180 Ectodomain Enables Prompt Diagnosis in a Subset of Patients
Growing evidence has linked bullous pemphigoid (BP) to immune checkpoint inhibitor (ICI) therapy in cancer treatment. However, the immunological features of ICI-associated BP (ICI-BP) are not yet fully elucidated. In order to characterize the humoral response in ICI BP patients and investigate whether their epitope profile differs from idiopathic BP (IBP), 53 ICI-BP patients were enrolled, immunologically characterized and compared with 59 IBP patients. ICI-BP had a distinctive IgG humoral profile, with reduced reactivity toward BP230 and recognition of multiple BP180 epitopes beyond the immunodominant extracellular noncollagenous 16A domain (NC16A). Specifically, reactivity to BP180 ectodomain was present in 94% of ICI-BP and 78% of IBP (p=0.044). Moreover, BP180 C-terminal epitope was more frequently targeted in ICI-BP than IBP (72% vs 41%, p=0.002). Notably, the combined use of an in-house BP180 ectodomain ELISA and the commercial BP180 test increased diagnostic sensitivity from 83% to 100%. Enhanced IgG reactivity toward nonimmunodominant epitopes, and especially C-terminal epitope recognition, characterize the humoral immune response in ICI-BP. Our data suggest that combining NC16A and fulllength BP180 ectodomain ELISAs may help reduce diagnostic delay in ICI-BP patients, in whom a timely diagnosis is crucial to appropriately manage the disease and ultimately avoid discontinuation ofcancer therapy.
Characterisation of the novel HLA‐DPA1*01:12:03 allele by sequencing‐based typing
HLA‐DPA1*01:12:03 differs from HLA‐DPA1*01:12:01 by one nucleotide substitution in codon 204 in exon 4.
Characterisation of the novel HLA‐DPA1*01:12:03 allele by sequencing‐based typing
HLA‐DPA1*01:12:03 differs from HLA‐DPA1*01:12:01 by one nucleotide substitution in codon 204 in exon 4.
Identification of the novel HLA‐C*07:1132 allele by next‐generation sequencing
The novel HLA‐C*07:1132 allele differs from HLA‐C*07:01:01 by one nucleotide substitution in Exon 5.
Identification of the novel HLA‐C*07:1132 allele by next‐generation sequencing
The novel HLA‐C*07:1132 allele differs from HLA‐C*07:01:01 by one nucleotide substitution in Exon 5.
HLA alleles associated to susceptibility to gliptin‐associated bullous pemphigoid in Italian patients
Bullous pemphigoid (BP), although a rare disease, is the most frequent subepidermal autoimmune disorder. Treatment with gliptins, used for type 2 diabetes, was reported as associated with BP onset. To identify HLA alleles that may reflect a higher susceptibility to BP in the Italian population, we analysed 30 patients affected by idiopathic bullous pemphigoid (IBP) and 86 gliptin‐associated BP (GABP) patients. A significant association between HLA‐DQB1*03:01 allele and IBP and GABP patients was found. Of note, both IBP and GABP were significantly associated with one of the following haplotypes: DRB1*11:01, DRB3*02:02, DQA1*05:05, DQB1*03:01 or DRB1*11:04, DRB3*02:02, DQA1*05:05 and DQB1*03:01. These data identify, for the first time, potential markers of susceptibility to BP in the Italian population, especially when associated with gliptin intake.
HLA alleles associated to susceptibility to gliptin‐associated bullous pemphigoid in Italian patients
Bullous pemphigoid (BP), although a rare disease, is the most frequent subepidermal autoimmune disorder. Treatment with gliptins, used for type 2 diabetes, was reported as associated with BP onset. To identify HLA alleles that may reflect a higher susceptibility to BP in the Italian population, we analysed 30 patients affected by idiopathic bullous pemphigoid (IBP) and 86 gliptin‐associated BP (GABP) patients. A significant association between HLA‐DQB1*03:01 allele and IBP and GABP patients was found. Of note, both IBP and GABP were significantly associated with one of the following haplotypes: DRB1*11:01, DRB3*02:02, DQA1*05:05, DQB1*03:01 or DRB1*11:04, DRB3*02:02, DQA1*05:05 and DQB1*03:01. These data identify, for the first time, potential markers of susceptibility to BP in the Italian population, especially when associated with gliptin intake.
Characterization of the novel HLA‐DRB3*02:192 allele by sequencing‐based typing
HLA‐DRB3*02:192 differs from DRB3*02:02:01:02 by one nucleotide substitution in codon 204 in exon 4.
Characterization of the novel HLA‐DRB3*02:192 allele by sequencing‐based typing
HLA‐DRB3*02:192 differs from DRB3*02:02:01:02 by one nucleotide substitution in codon 204 in exon 4.
- Open Access
Characterization of the novel HLA‐DQA1*05:05:14 allele by sequencing‐based typing
HLA‐DQA1*05:05:14 differs from HLA‐DQA1*05:05:01:04 by one nucleotide substitution in codon −8 in exon 1.
Open AccessCharacterization of the novel HLA‐DQA1*05:05:14 allele by sequencing‐based typing
HLA‐DQA1*05:05:14 differs from HLA‐DQA1*05:05:01:04 by one nucleotide substitution in codon −8 in exon 1.
Characterization of the novel HLA‐DPA1*01:03:40 allele by sequencing‐based typing
HLA‐DPA1*01:03:40 differs from HLA‐DPA1*01:03:01:02 by one nucleotide substitution in codon 60 in exon 2.
Characterization of the novel HLA‐DPA1*01:03:40 allele by sequencing‐based typing
HLA‐DPA1*01:03:40 differs from HLA‐DPA1*01:03:01:02 by one nucleotide substitution in codon 60 in exon 2.
A new HLA‐B allele, HLA‐B*07:422
The novel allele HLA‐B*07:422 differs from HLA‐B*07:02:01:01 by one nucleotide substitution in exon 4.
A new HLA‐B allele, HLA‐B*07:422
The novel allele HLA‐B*07:422 differs from HLA‐B*07:02:01:01 by one nucleotide substitution in exon 4.
Characterization of the novel HLA‐DQA1*01:02:11 allele by sequencing‐based typing
HLA‐DQA1*01:02:11 differs from HLA‐DQA1*01:02:01:10 by one nucleotide substitution in codon 201 in exon 4.
Characterization of the novel HLA‐DQA1*01:02:11 allele by sequencing‐based typing
HLA‐DQA1*01:02:11 differs from HLA‐DQA1*01:02:01:10 by one nucleotide substitution in codon 201 in exon 4.
Characterization of the novel HLA‐DQA1*01:58 allele by sequencing‐based typing
HLA‐DQA1*01:58 differs from HLA‐DQA1*01:02:01:06 by one nucleotide substitution in codon 46 in exon 2.
Characterization of the novel HLA‐DQA1*01:58 allele by sequencing‐based typing
HLA‐DQA1*01:58 differs from HLA‐DQA1*01:02:01:06 by one nucleotide substitution in codon 46 in exon 2.