Parvovirus B19 (B19V) is a contagious virus. It is responsible for a wide range of clinical manifestations, from spontaneously resolving illness to potentially fatal and severe conditions in at risk individuals such as pregnant women. This study would enable the investigation of clinical and biological manifestations as well as adverse fetal outcomes in pregnant women with recent infection. We reported a series of 16 pregnant women with primary B19V infection. Diagnosis was clinical, serological, and molecular. Real-time PCR molecular analysis was performed on all pregnant women with recent B19V infection. Viral DNA was detected in 3 women. Mothers with recent B19V infection were symptomatic in 68.75% (11/16) of cases, and 62.5% (10/16) had developed arthralgia associated with a rash. Anemia was present in half the women with recent infection, with only one case of thrombocytopenia. Postnatal follow-up of the infected mothers showed that 13 women gave birth to healthy new borns. Two patients experienced a spontaneous abortion, and another gave birth to a premature infant. Given the complications of B19V infection, the assessment of maternal infection is important and should be considered within the framework of the fetal and maternal health policy in Morocco.

Chimeric antigen receptor (CAR) T-cell therapy has revolutionized the treatment of B-cell malignancies and has attracted growing interest for autoimmune and allergic diseases. Because these disorders are often driven by pathogenic B cells that produce autoantibodies or allergen-specific IgE, they represent promising targets for CAR-T–based therapies. Studies have demonstrated that CD19-targeted CAR-T cells can induce deep and sustained drug-free remissions in severe autoimmune diseases, including systemic lupus erythematosus, idiopathic inflammatory myositis, and systemic sclerosis. Early evidence from multiple independent centers now extending to 36 months of follow-up indicates that CAR-T therapy may enable long-term disease control and potentially curative outcomes in carefully selected patients, rather than merely alleviating symptoms. Concurrently, preclinical research is advancing CAR-T approaches for allergic diseases, with efforts focused on eliminating IgE-producing B cells and engineering regulatory CAR-T cells to restore immune tolerance. In this review, we synthesized the mechanisms underlying CAR-T function, along with emerging preclinical data and clinical outcomes supporting its use in immune-mediated disorders. We also explored innovative strategies, including chimeric autoantibody receptor (CAAR) T cells, dual-targeting constructs, and next-generation CAR designs incorporating safety switches to improve efficacy and minimize toxicity. Despite promising early results, several challenges remain, including limited long-term safety data, the need for standardized patient selection criteria, manufacturing complexity, and questions regarding optimal timing and disease stage for intervention. Continued advances in cell engineering and scalable production are expected to address these limitations. Overall, CAR-T therapy represents a promising and potentially transformative approach for treating refractory autoimmune and allergic diseases.

Tuberculosis (TB) is an infectious disease, particularly preventable in children using the Bacillus Calmette-Guérin (BCG) attenuated vaccine. Individuals with strong immune systems can safely receive the BCG vaccine; however, certain factors such as age, immune system problems, vaccine dose, and injection route can cause side effects. Mild local reactions and ulceration at the intradermal injection site are common after BCG vaccination. However, in individuals with weakened immune systems, serious complications such as suppurative lymphadenitis, osteitis, or disseminated BCG disease (BCGosis) may develop. Therefore, the BCG vaccine should be carefully considered in individuals infected with human immunodeficiency virus (HIV) and patients with primary immunodeficiency disorder (PID). Treatment methods depend on the severity of the condition. In cases of uncomplicated injection site ulceration and minor, non-suppurative lymphadenopathy, local wound care and observation are conservative treatments. However, management approaches for deep or disseminated disease include surgical interventions and antimycobacterial therapy in addition to immunological evaluation. Furthermore, while hematopoietic stem cell transplantation may be considered in some PID patients, urgent enzyme replacement therapy using polyethylene glycol–modified adenosine deaminase (ADA) is necessary in patients with ADA deficiency. In conclusion, the BCG vaccine is a powerful tool in preventing TB, especially in childhood, and is safe in people with healthy immune systems. However, in individuals with any immune system–related disease, the administration of this attenuated vaccine should be evaluated by specialist physicians, and immediate intervention should be sought in case of serious side effects.

Background: Ataxia-telangiectasia (A-T) is a rare, autosomal recessive, multisystem disorder caused by mutations in the ATM gene. Atypical presentations that lack classic ocular telangiectasias or present predominantly with early-onset movement disorders pose significant diagnostic challenges and frequently lead to misdiagnosis during early childhood. Case Presentation: We reported a 6-year-old Chinese boy who was presented with delayed motor milestones and dysarthria since 1 year of age. Brain magnetic resonance imaging (MRI) revealed distinct cerebellar atrophy. Notably, classic oculocutaneous telangiectasias were absent; instead, atypical hypopigmented macules were observed on the skin. Whole-exome sequencing identified compound heterozygous mutations in the ATM gene: A known pathogenic missense variant (c.8110T>G) and a novel, maternally inherited frameshift mutation (c.3613dup, p.Arg1205Profs*24) were found in exon 25. In silico analysis predicted that this novel variant triggers nonsense-mediated mRNA decay (NMD), potentially leading to loss of the ATM protein kinase catalytic domain, which aligns with his mild- to-moderate neurological and severe immunological phenotypes. Conclusion: This case highlights that progressive cerebellar involvement and profound immunological compromise can manifest in A-T patients even in the absence of classic telangiectasias. The identification of the novel c.3613dup mutation broadens the genotypic spectrum of the ATM gene. Furthermore, it underscores the critical importance of integrating early genetic screening for atypical childhood- onset movement disorders to prevent diagnostic delays and facilitate timely multidisciplinary management.

Background and objectives: Systemic lupus erythematosus (SLE) is a chronic autoimmune disease frequently complicated by renal involvement, known as lupus nephritis (LN). Pentraxin 3 (PTX3) is an acute-phase protein implicated in immune regulation, and autoantibodies against PTX3 (anti-PTX3) have been hypothesized to exert a protective effect against the development of LN in SLE patients. The objective of the current study was to evaluate serum levels of anti-PTX3 IgG and anti-double-stranded DNA (anti-dsDNA) IgG antibodies in SLE patients and to assess their association with disease activity and proteinuria. Methods: This cross-sectional study included 69 participants divided into three groups: SLE patients with proteinuria, SLE patients without proteinuria, and healthy controls. Serum IgG anti-PTX3 and anti-dsDNA levels were measured using enzyme-linked immunosorbent assay (ELISA). Proteinuria was assessed by measuring the albumin-to-creatinine ratio (A/Cr). Associations between antibody levels, proteinuria, and disease activity index were analyzed. Results: Serum anti-PTX3 levels were highest in SLE patients without proteinuria, with a statistically significant difference among the three groups ( p = 0.031). Anti-dsDNA antibodies were detected exclusively in SLE patients; however, no significant difference was observed between patients with and without proteinuria ( p = 1.00). Anti-PTX3 levels demonstrated a weak negative correlation with A/Cr (r = −0.082) and with disease activity index (r = −0.142). Conclusions: Higher anti-PTX3 levels in SLE patients without proteinuria and their inverse relationship with proteinuria and disease activity were observed in this cross-sectional sample; however, these correlations were weak and not statistically significant, and a protective or causal role cannot be established from these data. Anti-PTX3 may represent a candidate marker warranting longitudinal validation in patients with SLE.