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Integration of CD200, CD43 and ROR1 in Multiparameter Flow Cytometry (MFC) Routine Panels for the Differential Diagnosis of B-cell lymphoproliferative Disorders (B-LPDs).
Mediterr J Hematol Infect Dis
January 2025
Hematology, Department of Translational and Precision Medicine, Sapienza University of Rome, Italy.
Background: Clonal mature B-cell lymphoproliferative disorders (B-LPDs) are a heterogeneous group of neoplasia characterized by the proliferation of mature B lymphocytes in the peripheral blood, bone marrow and/or lymphoid tissues. B-LPDs classification into different subtypes and their diagnosis is based on a multiparametric approach. However, accurate diagnosis may be challenging, especially in cases of ambiguous interpretation.
View Article and Find Full Text PDFThe CD4 T cell-independent IgG response during persistent virus infection favors emergence of neutralization-escape variants.
bioRxiv
December 2024
Department of Microbiology and Immunology, Penn State College of Medicine, Hershey, PA 17033, USA.
How changes in the quality of anti-viral antibody (Ab) responses due to pre-existing or acquired CD4 T cell insufficiency affect virus evolution during persistent infection are unknown. Using mouse polyomavirus (MuPyV), we found that CD4 T cell depletion before infection results in short-lived plasma cells secreting low-avidity antiviral IgG with limited BCR diversity and weak virus-neutralizing ability. CD4 T cell deficiency during persistent infection incurs a shift from a T-dependent (TD) to T-independent (TI) Ab response, resembling the pre-existing TI Ab response.
View Article and Find Full Text PDFHeightened innate immune state induced by viral vector leads to enhanced response to challenge and prolongs malaria vaccine protection.
iScience
December 2024
Department of Internal Medicine, Division of Infectious Diseases, University of Texas Medical Branch, Galveston, TX 77555-0435, USA.
Cytomegalovirus is a promising vaccine vector; however, mechanisms promoting CD4 T cell responses to challenge, by CMV as a vector, are unknown. The ability of MCMV to prolong immunity generated by short-lived malaria vaccine was tested. MCMV provided non-specific protection to challenge with and increased interleukin-12 (IL-12) and CD8α dendritic cell (DC) numbers through prolonged MCMV-dependent interferon gamma (IFN-γ) production.
View Article and Find Full Text PDFTetraspanin CD81 serves as a functional entry factor for porcine circovirus type 2 infection.
J Virol
December 2024
Key Laboratory of Animal Disease Diagnostics and Immunology, Ministry of Agriculture, MOE International Joint Collaborative Research Laboratory for Animal Health & Food Safety, College of Veterinary Medicine, Nanjing Agricultural University, Nanjing, Jiangsu, China.
Porcine circovirus type 2 (PCV2) is the primary causative agent of porcine circovirus-associated disease, clinically resulting in immunosuppression and co-infections with other pathogens in infected pigs. The mechanism of PCV2 infection remains unclear. In this study, we firstly found that the tetraspanin CD81 in PK-15 cells interacts with PCV2 Cap protein by using virus overlay protein-binding assay combined with mass spectrometry.
View Article and Find Full Text PDFNaturally arising memory-phenotype CD4 T lymphocytes contain an undifferentiated population that can generate T1, T17, and T cells.
Sci Adv
December 2024
Department of Microbiology and Immunology, Tohoku University Graduate School of Medicine, Sendai, Miyagi, Japan.
Article Synopsis
- Memory-phenotype (MP) CD4 T lymphocytes develop from naïve T cells and can differentiate into various T cell subsets to manage inflammation, especially in low-immune settings.
- The study highlights that MP lymphocytes are not only made up of T helper 1 (T1) and T helper 17 (T17) cells but also contain a "undifferentiated" subpopulation that has the potential to develop into these functional subsets.
- The undifferentiated MP lymphocytes possess the ability to proliferate rapidly and can differentiate into T1, T17, and regulatory T cells, which contributes to inflammation, although their response is regulated by existing T cells.
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